@article {1411060, title = {Microstructures amplify carotenoid plumage signals in tanagers.}, journal = {Sci Rep}, volume = {11}, year = {2021}, author = {McCoy, D.E. and Shultz, A. J. and Vidoudez, C. and et al.} } @article {1417381, title = {Poles apart: monosporic, bisporic, and tetrasporic embryo sacs revisited.}, journal = {Frontiers in Ecology and Evolution}, volume = {8}, year = {2020}, pages = {516640}, author = {Haig, D.} } @article {1411072, title = {On the logic of Fisherian sexual selection*}, journal = {Evolution}, volume = {74}, year = {2020}, pages = {1234-1245}, url = {https://doi.org/10.1111/evo.13944}, author = {Veller, C. and Muralidhar, P. and Haig, D.} } @article {1411064, title = {The Evolution of Imprinted microRNAs and Their RNA Targets}, journal = {Genes}, volume = {11}, year = {2020}, url = {https://doi.org/10.3390/genes11091038}, author = {Haig, D. and Mainieri, A.} } @article {1411061, title = {Embryo Selection and Mate Choice: Can {\textquoteleft}Honest Signals{\textquoteright} Be Trusted?}, journal = {Trends in Ecology \& Evolution}, volume = {35}, year = {2020}, pages = {308-318}, url = {https://www.sciencedirect.com/science/article/pii/S0169534719303441}, author = {McCoy, Dakota E. and Haig, David} } @article {1411070, title = {Response to vocal music in Angelman syndrome contrasts with Prader-Willi syndrome}, journal = {Evolution and Human Behavior}, volume = {40}, year = {2019}, pages = {420-426}, url = {https://doi.org/10.1016/j.evolhumbehav.2019.05.003.}, author = {Jennifer Kotler and Samuel A. Mehr and Alena Egner and Haig, David and Max M. Krasnow} } @article {1411067, title = {Retrotransposon gag-like 1 (RTL1) and the molecular evolution of self-targeting imprinted microRNAs.}, journal = {Biol Direct}, volume = {14}, year = {2019}, url = {https://doi.org/10.1186/s13062-019-0250-0}, author = {Mainieri, A. and Haig, D.} } @article {1411063, title = {A comparative study of litter size and sex composition in a large data set of callitrichine monkeys.}, journal = {Am J Primatol.}, volume = {81:}, year = {2019}, url = {https://doi.org/10.1002/ajp.23038}, author = {McCoy, DE and Frye, BM and Kotler, J and et al.} } @article {1411062, title = {Cooperation and conflict in human pregnancy}, journal = {Current Biology}, volume = {29}, year = {2019}, pages = {R455-R458}, author = {Haig, David} } @article {1411059, title = {Structurally assisted super black in colourful peacock spiders.}, journal = {spidersProc. R. Soc. B.}, volume = {286}, year = {2019}, author = {McCoy, DE and McCoy, VE and Mandsberg, NK and Shneidman, AV and Aizenberg, J and Prum, RO and Haig, D.} } @article {1417386, title = {Female babies and risk aversion: causal evidence from hospital wards}, journal = {Journal of Health Economics }, volume = {58}, year = {2018}, pages = {10-17}, author = {G Pogrebna and AJ Oswald and Haig, D.} } @article {1417385, title = {Lost in translation: the 3{\textquoteright}-UTR of IGF1R as a long noncoding RNA}, journal = {Evolution, Medicine and Public Health}, volume = { 2018}, year = {2018}, pages = {82{\textendash}91}, author = {A Mainieri and Haig, D.} } @article {1411066, title = {The tempo of human childhood: a maternal foot on the accelerator, a paternal foot on the brake.}, journal = {Evolutionary Anthropology.}, volume = {27}, year = {2018}, pages = {80{\textendash}91}, url = {https://doi.org/10.1002/evan.21579}, author = {Kotler, J. and Haig, D.} } @article {1417395, title = {Sexy males and sexless females: the origin of triploid apomicts}, journal = {Heredity}, volume = {118}, year = {2017}, pages = {436{\textendash}441}, author = {P Muralidhar and Haig, D.} } @article {1417392, title = {Genomic imprinting is implicated in the psychology of music}, journal = {Psychological Science}, volume = {28}, year = {2017}, pages = {1455{\textendash}1467}, author = {SA Mehr and Kotler, J and RM Howard and Haig, D.} } @article {1417391, title = {Paternally inherited DLK1 deletion associated with familial central precocious puberty}, journal = {Journal of Clinical Endocrinology and Metabolism }, volume = {102}, year = {2017}, pages = {1557{\textendash}1567}, author = {A Dauber and M Cunha-Silva and DB Macedo and VN Brito and AP Abreu and SA Roberts and LR Montenegro and M Andrew and A Kirby and MT Weirauch and G Labilloy and DS Bessa and RS Carroll and DC Jacobs and PE Chappell and B Mendonca and Haig, D. and UB Kaiser and AC Latronico} } @article {1417402, title = {The Trivers{\textendash}Willard hypothesis: sex ratio or investment? }, journal = {Proceedings of the Royal Society B}, volume = {283}, year = {2016}, pages = {20160126}, author = {C Veller and Haig, D. and MA Nowak} } @article {1417401, title = {Nutritional phases in Prader{\textendash}Willi syndrome: evolutionary and clinical interpretations}, journal = {Journal of Evolutionary Medicine}, volume = {4}, year = {2016}, pages = {235968}, author = {Kotler, J and K Balko and G Berall and Haig, D.} } @article {1417400, title = {Sleeping Beauty in a grain of rice}, journal = {Biology \& Philosophy}, volume = {31}, year = {2016}, pages = {23{\textendash}37}, author = {Haig, D.} } @article {1417399, title = {Intracellular evolution of mitochondrial DNA (mtDNA) and the tragedy of the cytoplasmic commons}, journal = {Bioessays}, volume = {38}, year = {2016}, pages = {549{\textendash}555}, author = {Haig, D.} } @article {1417397, title = {Living together and living apart: the sexual lives of bryophytes}, journal = {Philosophical Transactions of the Royal Society of London B }, volume = {371}, year = {2016}, pages = {20150535}, author = {Haig, D.} } @article {1417396, title = {Transposable elements: self-seekers of the germline, team players of the soma}, journal = {Bioessays}, volume = {38}, year = {2016}, pages = {1158{\textendash}1166}, author = {Haig, D.} } @article {1417405, title = {Coleochaete and the origin of sporophytes}, journal = {American Journal of Botany}, volume = {102}, year = {2015}, pages = {417{\textendash}422}, author = {Haig, D.} } @article {1417404, title = {Maternal-fetal conflict, genomic imprinting, and mammalian vulnerabilities to cancer}, journal = {Philosophical Transactions of the Royal Society of London B}, volume = {370}, year = {2015}, pages = {20140178}, author = {Haig, D.} } @article {1417403, title = {Sameness, novelty, and nominal kinds}, journal = {Biology \& Philosophy }, volume = {30}, year = {2015}, pages = {857{\textendash}872}, author = {Haig, D.} } @article {508976, title = {Coadaptation and conflict, misconception and muddle, in the evolution of genomic imprinting}, journal = {Heredity (Edinb)}, volume = {113}, number = {2}, year = {2014}, note = {

Haig, DengEngland2013/10/17 06:00Heredity (Edinb). 2014 Aug;113(2):96-103. doi: 10.1038/hdy.2013.97. Epub 2013 Oct 16.

}, month = {Aug}, pages = {96-103}, abstract = {

Common misconceptions of the {\textquoteright}parental conflict{\textquoteright} theory of genomic imprinting are addressed. Contrary to widespread belief, the theory defines conditions for cooperation as well as conflict in mother-offspring relations. Moreover, conflict between genes of maternal and paternal origin is not the same as conflict between mothers and fathers. In theory, imprinting can evolve either because genes of maternal and paternal origin have divergent interests or because offspring benefit from a phenotypic match, or mismatch, to one or other parent. The latter class of models usually require maintenance of polymorphism at imprinted loci for the maintenance of imprinted expression. The conflict hypothesis does not require maintenance of polymorphism and is therefore a more plausible explanation of evolutionarily conserved imprinting.

}, isbn = {1365-2540 (Electronic)0018-067X (Linking)}, author = {Haig, D.} } @article {508956, title = {Does microchimerism mediate kin conflicts?}, journal = {Chimerism}, volume = {5}, number = {2}, year = {2014}, note = {

Haig, DavidENG2014/05/09 06:00Chimerism. 2014 May 8;5(2).

}, month = {May 8}, abstract = {

Fetal microchimerism (FMc) is predicted to promote the fitness of the fetus and maternal microchimerism (MMc) to promote the fitness of the mother. Offspring and mothers benefit from each other{\textquoteright}s health. Therefore, microchimeric cells should usually not be harmful to their host. However, the evolutionary interests of mothers and offspring diverge when there is competition among siblings for maternal investment. Fetal cells in mothers{\textquoteright} bodies could benefit their own offspring at the expense of its sibs by promoting lactogenesis or by extending the interbirth interval. Maternal cells in fetal bodies could benefit from the suppression of sibling rivalry. Non-inherited haplotypes in MMc or sibling microchimerism (SMc) gain no direct benefit from their hosts{\textquoteright} health and could be associated with substantial detrimental effects.

}, isbn = {1938-1964 (Electronic)1938-1964 (Linking)}, author = {Haig, D.} } @article {508651, title = {The evolution of reproduction-related NLRP genes}, journal = {J Mol Evol}, volume = {78}, number = {3-4}, year = {2014}, note = {

Duenez-Guzman, Edgar AHaig, DavidengHoward Hughes Medical Institute/Research Support, Non-U.S. Gov{\textquoteright}tGermany2014/03/13 06:00J Mol Evol. 2014 Apr;78(3-4):194-201. doi: 10.1007/s00239-014-9614-3. Epub 2014 Mar 11.

}, month = {Apr}, pages = {194-201}, abstract = {

NLRP proteins are important components of inflammasomes with a major role in innate immunity. A subset of NLRP genes, with unknown functions, are expressed in oocytes and early embryos. Mutations of Nlrp5 in mice are associated with maternal-effect embryonic lethality and mutations of NLRP7 in women are associated with conception of biparental complete hydatidiform moles (biCHMs), suggesting perturbed processes of genomic imprinting. Recessive mutations on NLRP2/7 in humans are associated with reproductive disorders and appear to be induced by a demethylation of the maternal pronucleus. In this study, we find that radiation of NLRP genes occurred before the common ancestor of Afrotheria and Boreoeutheria, with the clade of oocyte-expressed genes originating before the divergence of marsupial and eutherian mammals. There have been multiple independent duplications of NLRP2 genes one of which produced the NLRP7 gene associated with biCHMs.

}, isbn = {1432-1432 (Electronic)0022-2844 (Linking)}, author = {Duenez-Guzman, E. A. and Haig, D.} } @article {508946, title = {Frugal fat or munificent muscle: genomic imprinting and metabolism}, journal = {BMC Biol}, volume = {12}, number = {1}, year = {2014}, note = {

Haig, DavidengEditorialEngland2015/01/01 06:00BMC Biol. 2014 Dec 31;12(1):772. doi: 10.1186/s12915-014-0104-2.

}, pages = {772}, abstract = {

Variation in body composition is a popular obsession. The culturally {\textquoteright}ideal{\textquoteright} body type is light on fat and heavy on muscle but the human population is collectively laying on fat. A new study finds antagonistic effects of two imprinted genes, Grb10 and Dlk1, on body composition in mice. These findings pose the question whether there is an evolutionary conflict between genes of maternal and paternal origin over the optimal proportions of body fat and lean muscle mass.See research article: http://www.biomedcentral.com/1741-7007/12/99.

}, isbn = {1741-7007 (Electronic)1741-7007 (Linking)}, author = {Haig, D.} } @article {508971, title = {Interbirth intervals: Intrafamilial, intragenomic and intrasomatic conflict}, journal = {Evol Med Public Health}, volume = {2014}, number = {1}, year = {2014}, note = {

Haig, DavidengEngland2014/02/01 06:00Evol Med Public Health. 2014 Jan;2014(1):12-7. doi: 10.1093/emph/eou002. Epub 2014 Jan 16.

}, month = {Jan}, pages = {12-7}, abstract = {

BACKGROUND AND OBJECTIVES: Interbirth intervals (IBIs) mediate a trade-off between child number and child survival. Life history theory predicts that the evolutionarily optimal IBI differs for different individuals whose fitness is affected by how closely a mother spaces her children. The objective of the article is to clarify these conflicts and explore their implications for public health. METHODOLOGY: Simple models of inclusive fitness and kin conflict address the evolution of human birth-spacing. RESULTS: Genes of infants generally favor longer intervals than genes of mothers, and infant genes of paternal origin generally favor longer IBIs than genes of maternal origin. CONCLUSIONS AND IMPLICATIONS: The colonization of maternal bodies by offspring cells (fetal microchimerism) raises the possibility that cells of older offspring could extend IBIs by interfering with the implantation of subsequent embryos.

}, isbn = {2050-6201 (Electronic)2050-6201 (Linking)}, author = {Haig, D.} } @article {508951, title = {Sexual selection: placentation, superfetation, and coercive copulation}, journal = {Curr Biol}, volume = {24}, number = {17}, year = {2014}, note = {

Haig, DavidengCommentEngland2014/09/10 06:00Curr Biol. 2014 Sep 8;24(17):R805-8. doi: 10.1016/j.cub.2014.07.039.

}, month = {Sep 8}, pages = {R805-8}, abstract = {

The evolution of placentas in poeciliid fishes is associated with conception of overlapping litters and male mating strategies becoming more coercive. Sperm competition in ovaries of multiply-inseminated females may favor fertilization of immature eggs during ongoing pregnancies.

}, isbn = {1879-0445 (Electronic)0960-9822 (Linking)}, author = {Haig, D.} } @article {509016, title = {Specialists and generalists: the sexual ecology of the genome}, journal = {Cold Spring Harb Perspect Biol}, volume = {6}, number = {9}, year = {2014}, note = {

Haig, DavidUbeda, FranciscoPatten, Manus Meng2014/07/26 06:00Cold Spring Harb Perspect Biol. 2014 Jul 24;6(9):a017525. doi: 10.1101/cshperspect.a017525.

}, month = {Sep}, pages = {a017525}, abstract = {

Sexual antagonism occurs when an allele is beneficial in one sex but costly in the other. Parental antagonism occurs when an allele is beneficial when inherited from one sex but costly when inherited from the other because of fitness interactions among kin. Sexual and parental antagonisms together define four genetic niches within the genome that favor different patterns of gene expression. Natural selection generates linkage disequilibrium among sexually and parentally antagonistic loci with male-beneficial alleles coupled to alleles that are beneficial when inherited from males and female-beneficial alleles coupled to alleles that are beneficial when inherited from females. Linkage disequilibrium also develops between sexually and parentally antagonistic loci and loci that influence sex determination. Genes evolve sex-specific expression to resolve sexual antagonism and evolve imprinted expression to resolve parental antagonism. Sex-specific chromosomes allow a gene to specialize in a single niche.

}, isbn = {1943-0264 (Electronic)}, author = {Haig, D. and Ubeda, F. and Patten, M. M.} } @article {508961, title = {Troubled sleep: A response to commentaries}, journal = {Evol Med Public Health}, volume = {2014}, number = {1}, year = {2014}, note = {

Haig, DavidengEngland2014/03/19 06:00Evol Med Public Health. 2014 Jan;2014(1):57-62. doi: 10.1093/emph/eou011. Epub 2014 Mar 14.

}, month = {Jan}, pages = {57-62}, isbn = {2050-6201 (Electronic)2050-6201 (Linking)}, author = {Haig, D.} } @article {508966, title = {Troubled sleep: Night waking, breastfeeding and parent-offspring conflict}, journal = {Evol Med Public Health}, volume = {2014}, number = {1}, year = {2014}, note = {

Haig, DavidengEngland2014/03/13 06:00Evol Med Public Health. 2014 Jan;2014(1):32-9. doi: 10.1093/emph/eou005. Epub 2014 Mar 7.

}, month = {Jan}, pages = {32-9}, abstract = {

Disrupted sleep is probably the most common complaint of parents with a new baby. Night waking increases in the second half of the first year of infant life and is more pronounced for breastfed infants. Sleep-related phenotypes of infants with Prader-Willi and Angelman syndromes suggest that imprinted genes of paternal origin promote greater wakefulness whereas imprinted genes of maternal origin favor more consolidated sleep. All these observations are consistent with a hypothesis that waking at night to suckle is an adaptation of infants to extend their mothers{\textquoteright} lactational amenorrhea, thus delaying the birth of a younger sib and enhancing infant survival.

}, isbn = {2050-6201 (Electronic)2050-6201 (Linking)}, author = {Haig, D.} } @article {508941, title = {Filial mistletoes: the functional morphology of moss sporophytes}, journal = {Ann Bot}, volume = {111}, number = {3}, year = {2013}, note = {

Haig, DavidengEngland2013/01/02 06:00Ann Bot. 2013 Mar;111(3):337-45. doi: 10.1093/aob/mcs295. Epub 2012 Dec 30.

}, month = {Mar}, pages = {337-45}, abstract = {

BACKGROUND: A moss sporophyte inherits a haploid set of genes from the maternal gametophyte to which it is attached and another haploid set of genes from a paternal gametophyte. Evolutionary conflict is expected between genes of maternal and paternal origin that will be expressed as adaptations of sporophytes to extract additional resources from maternal gametophytes and adaptations of maternal gametophytes to restrain sporophytic demands. INTERPRETATION: The seta and stomata of peristomate mosses are interpreted as sporophytic devices for increasing nutrient transfer. The seta connects the foot, where nutrients are absorbed, to the developing capsule, where nutrients are needed for sporogenesis. Its elongation lifts stomata of the apophysis above the boundary layer, into the zone of turbulent air, thereby increasing the transpirational pull that draws nutrients across the haustorial foot. The calyptra is interpreted as a gametophytic device to reduce sporophytic demands. The calyptra fits tightly over the intercalary meristem of the sporophytic apex and prevents lateral expansion of the meristem. While intact, the calyptra delays the onset of transpiration. PREDICTIONS: Nutrient transfer across the foot, stomatal number and stomatal aperture are predicted to be particular arenas of conflict between sporophytes and maternal gametophytes, and between maternal and paternal genomes of sporophytes.

}, keywords = {*Genes, Plant, Adaptation, Physiological, Biological Transport, Bryophyta/*anatomy \& histology/classification/genetics/metabolism, Evolution, Molecular, Germ Cells, Plant/metabolism, Inheritance Patterns, Meristem/metabolism, Phylogeny, Plant Stomata/genetics/*metabolism, Plant Transpiration, Reproduction/genetics, Species Specificity}, isbn = {1095-8290 (Electronic)0305-7364 (Linking)}, author = {Haig, D.} } @article {508931, title = {Genomic vagabonds: endogenous retroviruses and placental evolution}, journal = {Bioessays}, volume = {35}, number = {10}, year = {2013}, note = {

Haig, DavidengComment2013/08/13 06:00Bioessays. 2013 Oct;35(10):845-6. doi: 10.1002/bies.201300099. Epub 2013 Aug 12.

}, month = {Oct}, pages = {845-6}, keywords = {*Evolution, Molecular, *Regulatory Sequences, Nucleic Acid, Animals, Endogenous Retroviruses/*genetics, Female, Humans, Placenta/*physiology, Pregnancy}, isbn = {1521-1878 (Electronic)0265-9247 (Linking)}, author = {Haig, D.} } @article {508926, title = {Imprinted green beards: a little less than kin and more than kind}, journal = {Biol Lett}, volume = {9}, number = {6}, year = {2013}, note = {

Haig, DavidengEngland2013/10/18 06:00Biol Lett. 2013 Oct 16;9(6):20130199. doi: 10.1098/rsbl.2013.0199. Print 2013.

}, pages = {20130199}, abstract = {

RNA is complementary to the DNA sequence from which it is transcribed. Therefore, interactions between DNA and RNA provide a simple mechanism of genetic self-detection within nuclei. Imprinted RNAs could enable alleles of maternal and paternal origin to detect whether they are the same (homozygous) or different (heterozygous), and thereby provide strategic information about expected relatedness to siblings.

}, keywords = {*Alleles, *Genomic Imprinting, Algorithms, Animals, DNA/*chemistry, Humans, Models, Genetic, Multigene Family, Mutation, Probability, RNA, Small Interfering/metabolism, RNA/*chemistry}, isbn = {1744-957X (Electronic)1744-9561 (Linking)}, author = {Haig, D.} } @article {508936, title = {Kin conflict in seed development: an interdependent but fractious collective}, journal = {Annu Rev Cell Dev Biol}, volume = {29}, year = {2013}, note = {

Haig, DavidengReview2013/05/07 06:00Annu Rev Cell Dev Biol. 2013;29:189-211. doi: 10.1146/annurev-cellbio-101512-122324. Epub 2013 Apr 29.

}, pages = {189-211}, abstract = {

Seeds are complex structures that unite diploid maternal tissues with filial tissues that may be haploid (gametophyte), diploid (embryo), or triploid (endosperm). Maternal tissues are predicted to favor smaller seeds than are favored by filial tissues, and filial genes of maternal origin are predicted to favor smaller seeds than are favored by filial genes of paternal origin. Consistent with these predictions, seed size is determined by an interplay between growth of maternal integuments, which limits seed size, and of filial endosperm, which promotes larger seeds. Within endosperm, genes of paternal origin favor delayed cellularization of endosperm and larger seeds, whereas genes of maternal origin favor early cellularization and smaller seeds. The ratio of maternal and paternal gene products in endosperm contributes to the failure of crosses between different ploidy levels of the same species and crosses between species. Maternally expressed small-interfering RNAs (siRNAs) are predicted to associate with growth-enhancing genes.

}, keywords = {Arabidopsis/genetics/metabolism, Endosperm/genetics, Gene Expression Regulation, Plant, Germ Cells, Plant/metabolism, Plant Development, Plants/*embryology/*genetics, Seeds/genetics/*growth \& development/physiology}, isbn = {1530-8995 (Electronic)1081-0706 (Linking)}, author = {Haig, D.} } @article {509651, title = {Proximate and ultimate causes: how come? and what for?}, journal = {Biol Philos}, volume = {28}, year = {2013}, pages = {781-786}, abstract = {

Proximate and ultimate causes in evolutionary biology have come to conflate two distinctions. The first is a distinction between immediate and historical causes. The second is between explanations of mechanism and adaptive function. Mayr emphasized the first distinction but many evolutionary biologists use proximate and ultimate causes to refer to the second. I recommend that {\textquoteleft}ultimate cause{\textquoteright} be abandoned as ambiguous.

}, url = {http://link.springer.com/article/10.1007\%2Fs10539-013-9369-z$\#$page-1}, author = {Haig, D.} } @article {509476, title = {Sexual and parental antagonism shape genomic architecture}, journal = {Proc Biol Sci}, volume = {280}, number = {1770}, year = {2013}, note = {

Patten, Manus MUbeda, FranciscoHaig, DavidengEngland2013/09/13 06:00Proc Biol Sci. 2013 Sep 11;280(1770):20131795. doi: 10.1098/rspb.2013.1795. Print 2013 Nov 7.

}, month = {Nov 7}, pages = {20131795}, abstract = {

Populations with two sexes are vulnerable to a pair of genetic conflicts: sexual antagonism that can arise when alleles have opposing fitness effects on females and males; and parental antagonism that arises when alleles have opposing fitness effects when maternally and paternally inherited. This paper extends previous theoretical work that found stable linkage disequilibrium (LD) between sexually antagonistic loci. We find that LD is also generated between parentally antagonistic loci, and between sexually and parentally antagonistic loci, without any requirement of epistasis. We contend that the LD in these models arises from the admixture of gene pools subject to different selective histories. We also find that polymorphism maintained by parental antagonism at one locus expands the opportunity for polymorphism at a linked locus experiencing parental or sexual antagonism. Taken together, our results predict the chromosomal clustering of loci that segregate for sexually and parentally antagonistic alleles. Thus, genetic conflict may play a role in the evolution of genomic architecture.

}, keywords = {*Genetic Fitness, *Linkage Disequilibrium, *Selection, Genetic, Alleles, Animals, Biological Evolution, Female, Male, Mating Preference, Animal, Models, Genetic, Polymorphism, Genetic}, isbn = {1471-2954 (Electronic)0962-8452 (Linking)}, author = {Patten, M. M. and Ubeda, F. and Haig, D.} } @article {508921, title = {Commentary: The epidemiology of epigenetics}, journal = {Int J Epidemiol}, volume = {41}, number = {1}, year = {2012}, note = {

Haig, DavidengCommentEngland2011/12/22 06:00Int J Epidemiol. 2012 Feb;41(1):13-6. doi: 10.1093/ije/dyr183. Epub 2011 Dec 20.

}, month = {Feb}, pages = {13-6}, keywords = {*Epigenesis, Genetic, *Genotype, *Phenotype, Animals, Drosophila melanogaster/*genetics}, isbn = {1464-3685 (Electronic)0300-5771 (Linking)}, author = {Haig, D.} } @article {508916, title = {Retroviruses and the placenta}, journal = {Curr Biol}, volume = {22}, number = {15}, year = {2012}, note = {

Haig, DavidengReviewEngland2012/08/11 06:00Curr Biol. 2012 Aug 7;22(15):R609-13. doi: 10.1016/j.cub.2012.06.002.

}, month = {Aug 7}, pages = {R609-13}, abstract = {

Retroviruses are often expressed in the placenta. Placental expression probably evolved to facilitate retroviral transmission from mother to offspring and from offspring to mother. In the process, the placenta became a site where retroviral genes were {\textquoteright}domesticated{\textquoteright} to serve adaptive functions in the host, including the manipulation of maternal physiology for the benefit of the fetus. The evolutionary interplay between retroviruses and host defenses may have contributed to the remarkable diversity of form among mammalian placentas and to mechanisms of genomic imprinting.

}, keywords = {Animals, Biological Evolution, Female, Genomic Imprinting, Humans, Infectious Disease Transmission, Vertical, Placenta/*virology, Pregnancy, Retroviridae/*physiology}, isbn = {1879-0445 (Electronic)0960-9822 (Linking)}, author = {Haig, D.} } @article {509686, title = {The strategic gene.}, journal = {Biol Philos}, volume = {27}, year = {2012}, pages = {461-479}, author = {Haig, D.} } @article {508911, title = {Does heritability hide in epistasis between linked SNPs?}, journal = {Eur J Hum Genet}, volume = {19}, number = {2}, year = {2011}, note = {

Haig, DavidengLetterEngland2010/10/07 06:00Eur J Hum Genet. 2011 Feb;19(2):123. doi: 10.1038/ejhg.2010.161. Epub 2010 Oct 6.

}, month = {Feb}, pages = {123}, keywords = {Body Height/genetics, Epistasis, Genetic/*genetics, Genetic Predisposition to Disease, Genome-Wide Association Study/*methods, Humans, Pedigree, Polymorphism, Single Nucleotide/*genetics}, isbn = {1476-5438 (Electronic)1018-4813 (Linking)}, author = {Haig, D.} } @article {509011, title = {Genomic imprinting: an obsession with depilatory mice}, journal = {Curr Biol}, volume = {21}, number = {7}, year = {2011}, note = {

Haig, DavidUbeda, FranciscoengEngland2011/04/13 06:00Curr Biol. 2011 Apr 12;21(7):R257-9. doi: 10.1016/j.cub.2011.02.027.

}, month = {Apr 12}, pages = {R257-9}, abstract = {

Excessive grooming in mice has been promoted as a model of human obsessive-compulsive disorders. A recent paper adds Grb10 to the list of genes with effects on behavioral hair loss, with the added twist that this time the gene is imprinted.

}, keywords = {*Genomic Imprinting, *Grooming, Animals, Disease Models, Animal, GRB10 Adaptor Protein/genetics, Humans, Mice, Obsessive-Compulsive Disorder/*genetics}, isbn = {1879-0445 (Electronic)0960-9822 (Linking)}, author = {Haig, D. and Ubeda, F.} } @article {508906, title = {Genomic imprinting and the evolutionary psychology of human kinship}, journal = {Proc Natl Acad Sci USA}, volume = {108 Suppl 2}, year = {2011}, note = {

Haig, DavidengHoward Hughes Medical Institute/Research Support, Non-U.S. Gov{\textquoteright}t2011/06/22 06:00Proc Natl Acad Sci U S A. 2011 Jun 28;108 Suppl 2:10878-85. doi: 10.1073/pnas.1100295108. Epub 2011 Jun 20.

}, month = {Jun 28}, pages = {10878-85}, abstract = {

Genomic imprinting is predicted to influence behaviors that affect individuals to whom an actor has different degrees of matrilineal and patrilineal kinship (asymmetric kin). Effects of imprinted genes are not predicted in interactions with nonrelatives or with individuals who are equally related to the actor{\textquoteright}s maternally and paternally derived genes (unless a gene also has pleiotropic effects on fitness of asymmetric kin). Long-term mating bonds are common in most human populations, but dissolution of marriage has always affected a significant proportion of mated pairs. Children born in a new union are asymmetric kin of children born in a previous union. Therefore, the innate dispositions of children toward parents and sibs are expected to be sensitive to cues of marital stability, and these dispositions may be subject to effects of imprinted genes.

}, keywords = {*Evolution, Molecular, *Genomic Imprinting, Family/*psychology, Humans, Models, Genetic}, isbn = {1091-6490 (Electronic)0027-8424 (Linking)}, author = {Haig, D.} } @article {509581, title = {Stable linkage disequilibrium owing to sexual antagonism}, journal = {Proc Biol Sci}, volume = {278}, number = {1707}, year = {2011}, note = {

Ubeda, FranciscoHaig, DavidPatten, Manus MengEngland2010/09/24 06:00Proc Biol Sci. 2011 Mar 22;278(1707):855-62. doi: 10.1098/rspb.2010.1201. Epub 2010 Sep 22.

}, month = {Mar 22}, pages = {855-62}, abstract = {

Linkage disequilibrium (LD) is an association between genetic loci that is typically transient. Here, we identify a previously overlooked cause of stable LD that may be pervasive: sexual antagonism. This form of selection produces unequal allele frequencies in males and females each generation, which upon admixture at fertilization give rise to an excess of haplotypes that couple male-beneficial with male-beneficial and female-beneficial with female-beneficial alleles. Under sexual antagonism, LD is obtained for all recombination frequencies in the absence of epistasis. The extent of LD is highest at low recombination and for stronger selection. We provide a partition of the total LD into distinct components and compare our result for sexual antagonism with Li and Nei{\textquoteright}s model of LD owing to population subdivision. Given the frequent observation of sexually antagonistic selection in natural populations and the number of traits that are often involved, these results suggest a major contribution of sexual antagonism to genomic structure.

}, keywords = {*Linkage Disequilibrium, *Models, Genetic, *Selection, Genetic, Animals, Female, Gene Frequency, Genotype, Male, Sex Factors}, isbn = {1471-2954 (Electronic)0962-8452 (Linking)}, author = {Ubeda, F. and Haig, D. and Patten, M. M.} } @article {509691, title = {Sympathy with Adam Smith and reflexions on self.}, journal = {J Econ Behav Org}, volume = {77}, year = {2011}, pages = {4-13}, author = {Haig, D.} } @article {508901, title = {Colloquium papers: Transfers and transitions: parent-offspring conflict, genomic imprinting, and the evolution of human life history}, journal = {Proc Natl Acad Sci USA}, volume = {107 Suppl 1}, year = {2010}, note = {

Haig, DavidengReview2009/08/12 09:00Proc Natl Acad Sci U S A. 2010 Jan 26;107 Suppl 1:1731-5. doi: 10.1073/pnas.0904111106. Epub 2009 Aug 4.

}, month = {Jan 26}, pages = {1731-5}, abstract = {

Human offspring are weaned earlier than the offspring of other great apes but take longer to reach nutritional independence. An analysis of human disorders of imprinted genes suggests genes of paternal origin, expressed in infants, have been selected to favor more intense suckling than genes of maternal origin. The same analysis suggests that genes of maternal origin may favor slower childhood growth but earlier sexual maturation. These observations are consistent with a hypothesis in which slow maturation was an adaptation of offspring that reduced maternal fitness, whereas early weaning was an adaptation of mothers that reduced the fitness of individual offspring.

}, keywords = {*Biological Evolution, *Genomic Imprinting, *Parent-Child Relations, Adaptation, Physiological, Child, Child Development, Female, Humans, Male, Puberty}, isbn = {1091-6490 (Electronic)0027-8424 (Linking)}, author = {Haig, D.} } @article {509471, title = {Fitness variation due to sexual antagonism and linkage disequilibrium}, journal = {Evolution}, volume = {64}, number = {12}, year = {2010}, note = {

Patten, Manus MHaig, DavidUbeda, Franciscoeng2010/08/21 06:00Evolution. 2010 Dec;64(12):3638-42. doi: 10.1111/j.1558-5646.2010.01100.x.

}, month = {Dec}, pages = {3638-42}, abstract = {

Extensive fitness variation for sexually antagonistic characters has been detected in nature. However, current population genetic theory suggests that sexual antagonism is unlikely to play a major role in the maintenance of variation. We present a two-locus model of sexual antagonism that is capable of explaining greater fitness variance at equilibrium than previous single-locus models. The second genetic locus provides additional fitness variance in two complementary ways. First, linked loci can maintain gene variants that are lost in single-locus models of evolution, expanding the opportunity for polymorphism. Second, linkage disequilibrium results between any two sexually antagonistic genes, producing an excess of high- and low-fitness haplotypes. Our results uncover a unique contribution of conflicting selection pressures to the maintenance of variation, which simpler models that neglect genetic architecture overlook.

}, keywords = {*Genetic Fitness, *Genetic Variation, Animals, Female, Haplotypes, Linkage Disequilibrium, Male, Models, Biological, Polymorphism, Genetic, Sex Characteristics}, isbn = {1558-5646 (Electronic)0014-3820 (Linking)}, author = {Patten, M. M. and Haig, D. and Ubeda, F.} } @article {508896, title = {Games in tetrads: segregation, recombination, and meiotic drive}, journal = {Am Nat}, volume = {176}, number = {4}, year = {2010}, note = {

Haig, Davideng2010/08/24 06:00Am Nat. 2010 Oct;176(4):404-13. doi: 10.1086/656265.

}, month = {Oct}, pages = {404-13}, abstract = {

The two alleles at a heterozygous locus segregate during meiosis, sometimes at meiosis I and sometimes at meiosis II. The timing of segregation is determined by the pattern of crossing-over between a locus and its attached centromeres. Genes near centromeres can exploit this process by driving against spores from which the genes separated at meiosis I. Other genes, located distal to centromeres, can benefit from driving against spores from which they separated at meiosis II. Asymmetric female meiosis is particularly susceptible to such forms of drive. Selection on modifiers of recombination favors changes in the location of chiasmata that increase the proportion of tetrads of high average fitness by changing the timing of segregation. Such changes increase the frequency of driving alleles. This source of selection on recombination does not depend on effects on linkage disequilibrium. Recombinational responses to meiotic drive may contribute to sex differences in overall recombination and sex differences in the localization of chiasmata.

}, keywords = {*Chromosome Segregation, *Meiosis, *Recombination, Genetic, Alleles, Genotype, Plants/*genetics}, isbn = {1537-5323 (Electronic)0003-0147 (Linking)}, author = {Haig, D.} } @article {508706, title = {High-resolution analysis of parent-of-origin allelic expression in the mouse brain}, journal = {Science}, volume = {329}, number = {5992}, year = {2010}, note = {

Gregg, ChristopherZhang, JiangwenWeissbourd, BrandonLuo, ShujunSchroth, Gary PHaig, DavidDulac, CatherineengHoward Hughes Medical Institute/Research Support, Non-U.S. Gov{\textquoteright}tNew York, N.Y.2010/07/10 06:00Science. 2010 Aug 6;329(5992):643-8. doi: 10.1126/science.1190830. Epub 2010 Jul 8.

}, month = {Aug 6}, pages = {643-8}, abstract = {

Genomic imprinting results in preferential expression of the paternal or maternal allele of certain genes. We have performed a genome-wide characterization of imprinting in the mouse embryonic and adult brain. This approach uncovered parent-of-origin allelic effects of more than 1300 loci. We identified parental bias in the expression of individual genes and of specific transcript isoforms, with differences between brain regions. Many imprinted genes are expressed in neural systems associated with feeding and motivated behaviors, and parental biases preferentially target genetic pathways governing metabolism and cell adhesion. We observed a preferential maternal contribution to gene expression in the developing brain and a major paternal contribution in the adult brain. Thus, parental expression bias emerges as a major mode of epigenetic regulation in the brain.

}, keywords = {*Gene Expression, *Genomic Imprinting, Alleles, Animals, Behavior, Animal, Brain/*embryology/growth \& development/*metabolism, Epigenesis, Genetic, Fathers, Female, Gene Expression Profiling, Gene Expression Regulation, Developmental, Gene Silencing, Male, Mice, Mothers, Multigene Family, Polymorphism, Single Nucleotide, Prefrontal Cortex/embryology/growth \& development/metabolism, Preoptic Area/embryology/growth \& development/metabolism, Sex Characteristics}, isbn = {1095-9203 (Electronic)0036-8075 (Linking)}, author = {Gregg, C. and Zhang, J. and Weissbourd, B. and Luo, S. and Schroth, G. P. and Haig, D. and Dulac, C.} } @article {508701, title = {Sex-specific parent-of-origin allelic expression in the mouse brain}, journal = {Science}, volume = {329}, number = {5992}, year = {2010}, note = {

Gregg, ChristopherZhang, JiangwenButler, James EHaig, DavidDulac, CatherineengHoward Hughes Medical Institute/Research Support, Non-U.S. Gov{\textquoteright}tNew York, N.Y.2010/07/10 06:00Science. 2010 Aug 6;329(5992):682-5. doi: 10.1126/science.1190831. Epub 2010 Jul 8.

}, month = {Aug 6}, pages = {682-5}, abstract = {

Genomic imprinting results in preferential gene expression from paternally versus maternally inherited chromosomes. We used a genome-wide approach to uncover sex-specific parent-of-origin allelic effects in the adult mouse brain. Our study identified preferential selection of the maternally inherited X chromosome in glutamatergic neurons of the female cortex. Moreover, analysis of the cortex and hypothalamus identified 347 autosomal genes with sex-specific imprinting features. In the hypothalamus, sex-specific imprinted genes were mostly found in females, which suggests parental influence over the hypothalamic function of daughters. We show that interleukin-18, a gene linked to diseases with sex-specific prevalence, is subject to complex, regional, and sex-specific parental effects in the brain. Parent-of-origin effects thus provide new avenues for investigation of sexual dimorphism in brain function and disease.

}, keywords = {*Alleles, *Epigenesis, Genetic, *Genes, X-Linked, *Genomic Imprinting, *Sex Characteristics, Animals, Crosses, Genetic, Dioxygenases, Female, Gene Expression Profiling, Glutamic Acid/metabolism, Interleukin-18/genetics, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Mitochondrial Proteins/genetics, Neurons/metabolism, Oxygenases/genetics, Polymorphism, Single Nucleotide, Prefrontal Cortex/cytology/*metabolism, Preoptic Area/cytology/*metabolism, Ribosomal Proteins/genetics, Succinate Dehydrogenase/genetics, X Chromosome Inactivation}, isbn = {1095-9203 (Electronic)0036-8075 (Linking)}, author = {Gregg, C. and Zhang, J. and Butler, J. E. and Haig, D. and Dulac, C.} } @article {509701, title = {Stable linkage disequilibrium owing to sexual antagonism.}, journal = {Proc Roy Soc Biol Sci}, volume = {278}, year = {2010}, pages = {855-862}, author = {Ubeda, F. and Haig, D. and Patten, M. M.} } @article {509706, title = {What do we know about charophyte (streptophyta) life cycles?}, journal = {J Phycol}, volume = {46}, year = {2010}, pages = {860-867}, author = {Haig, D.} } @article {509441, title = {Ancient origin of placental expression in the growth hormone genes of anthropoid primates}, journal = {Proc Natl Acad Sci USA}, volume = {106}, number = {40}, year = {2009}, note = {

Papper, ZackJameson, Natalie MRomero, RobertoWeckle, Amy LMittal, PoojaBenirschke, KurtSantolaya-Forgas, JoaquinUddin, MonicaHaig, DavidGoodman, MorrisWildman, Derek EengResearch Support, N.I.H., IntramuralResearch Support, U.S. Gov{\textquoteright}t, Non-P.H.S.2009/10/07 06:00Proc Natl Acad Sci U S A. 2009 Oct 6;106(40):17083-8. doi: 10.1073/pnas.0908377106. Epub 2009 Sep 18.

}, month = {Oct 6}, pages = {17083-8}, abstract = {

In anthropoid primates, growth hormone (GH) genes have undergone at least 2 independent locus expansions, one in platyrrhines (New World monkeys) and another in catarrhines (Old World monkeys and apes). In catarrhines, the GH cluster has a pituitary-expressed gene called GH1; the remaining GH genes include placental GHs and placental lactogens. Here, we provide cDNA sequence evidence that the platyrrhine GH cluster also includes at least 3 placenta expressed genes and phylogenetic evidence that placenta expressed anthropoid GH genes have undergone strong adaptive evolution, whereas pituitary-expressed GH genes have faced strict functional constraint. Our phylogenetic evidence also points to lineage-specific gene gain and loss in early placental mammalian evolution, with at least three copies of the GH gene present at the time of the last common ancestor (LCA) of primates, rodents, and laurasiatherians. Anthropoid primates and laurasiatherians share gene descendants of one of these three copies, whereas rodents and strepsirrhine primates each maintain a separate copy. Eight of the amino-acid replacements that occurred on the lineage leading to the LCA of extant anthropoids have been implicated in GH signaling at the maternal-fetal interface. Thus, placental expression of GH may have preceded the separate series of GH gene duplications that occurred in catarrhines and platyrrhines (i.e., the roles played by placenta-expressed GHs in human pregnancy may have a longer evolutionary history than previously appreciated).

}, keywords = {*Evolution, Molecular, *Phylogeny, Amino Acid Sequence, Animals, Catarrhini/classification/genetics, DNA, Complementary/chemistry/genetics, Female, Gene Expression Profiling, Gene Library, Growth Hormone/*genetics, Humans, Models, Genetic, Molecular Sequence Data, Mutation, Placenta/*metabolism, Platyrrhini/classification/genetics, Pregnancy, Primates/classification/*genetics, Selection, Genetic, Sequence Analysis, DNA, Sequence Homology, Nucleic Acid}, isbn = {1091-6490 (Electronic)0027-8424 (Linking)}, author = {Papper, Z. and Jameson, N. M. and Romero, R. and Weckle, A. L. and Mittal, P. and Benirschke, K. and Santolaya-Forgas, J. and Uddin, M. and Haig, D. and Goodman, M. and Wildman, D. E.} } @article {509461, title = {Maintenance or loss of genetic variation under sexual and parental antagonism at a sex-linked locus}, journal = {Evolution}, volume = {63}, number = {11}, year = {2009}, note = {

Patten, Manus MHaig, DavidengResearch Support, U.S. Gov{\textquoteright}t, Non-P.H.S.2009/07/04 09:00Evolution. 2009 Nov;63(11):2888-95. doi: 10.1111/j.1558-5646.2009.00764.x. Epub 2009 Jul 1.

}, month = {Nov}, pages = {2888-95}, abstract = {

An intralocus genetic conflict occurs when a locus is selected in opposing directions in different subsets of a population. Populations with two sexes have the potential to host a pair of distinct intralocus conflicts: sexual antagonism and parental antagonism. In this article, we examine the population genetic consequences of these conflicts for X-linked genes. Both conflicts are capable of maintaining genetic variation in a population, but to different degrees. For weak sexual antagonism, the X chromosome has a higher opportunity for polymorphism than the autosomes. For parental antagonism, there is a very limited opportunity for polymorphism on the X chromosome relative to autosomes or to sexual antagonism. X-linkage introduces an asymmetry in the inheritance and expression of sexually and parentally antagonistic genes that leads to a biased fixation of alleles with certain effects. We find little support for the commonly held intuition that the X chromosome should be biased toward fixing female-beneficial alleles. Contrary to this intuition, we find that the X chromosome is biased toward fixation of male-beneficial alleles for much of the range of dominance. Additionally, we find that the X chromosome is more favorable to the fixation of alleles that are beneficial when maternally derived.

}, keywords = {*Genetic Linkage, *Genetic Variation, *Sexual Behavior, Animal, *X Chromosome, Animals, Female, Male, Polymorphism, Genetic, Population dynamics}, isbn = {1558-5646 (Electronic)0014-3820 (Linking)}, author = {Patten, M. M. and Haig, D.} } @article {509466, title = {Parental sex discrimination and intralocus sexual conflict}, journal = {Biol Lett}, volume = {5}, number = {5}, year = {2009}, note = {

Patten, Manus MHaig, DavidengEngland2009/05/14 09:00Biol Lett. 2009 Oct 23;5(5):667-70. doi: 10.1098/rsbl.2009.0230. Epub 2009 May 12.

}, month = {Oct 23}, pages = {667-70}, abstract = {

Intralocus sexual conflict occurs when populations segregate for alleles with opposing fitness consequences in the two sexes. This form of selection is known to be capable of maintaining genetic and fitness variation in nature, the extent of which is sensitive to the underlying genetics. We present a one-locus model of a haploid maternal effect that has sexually antagonistic consequences for offspring. The evolutionary dynamics of these maternal effects are distinct from those of haploid direct effects under sexual antagonism because the relevant genes are expressed only in females. Despite this, we find the same opportunity for sexually antagonistic polymorphism at the maternal effect locus as at a direct effect locus. Thus, sexually antagonistic maternal effects may underlie some natural genetic variation. The model we present permits alternative interpretations of how the genes are expressed and how the fitness variation is assigned, which invites a theoretical comparison to models of both imprinted genes and sex allocation.

}, keywords = {*Models, Genetic, *Selection, Genetic, Alleles, Animals, Biological Evolution, Female, Genetic Variation, Genotype, Haploidy, Male, Plant Development, Plants/*genetics, Reproduction, Sex Factors}, isbn = {1744-957X (Electronic)1744-9561 (Linking)}, author = {Patten, M. M. and Haig, D.} } @article {509341, title = {Flt1, pregnancy, and malaria: evolution of a complex interaction}, journal = {Proc Natl Acad Sci USA}, volume = {105}, number = {38}, year = {2008}, note = {

Karumanchi, S AnanthHaig, DavidengHoward Hughes Medical Institute/CommentResearch Support, Non-U.S. Gov{\textquoteright}t2008/09/20 09:00Proc Natl Acad Sci U S A. 2008 Sep 23;105(38):14243-4. doi: 10.1073/pnas.0807932105. Epub 2008 Sep 18.

}, month = {Sep 23}, pages = {14243-4}, keywords = {*Biological Evolution, Animals, Female, Fetal Death/etiology, Gene Frequency, Humans, Malaria, Falciparum/complications/*genetics, Placenta/parasitology, Polymorphism, Genetic, Pregnancy, Pregnancy Complications, Parasitic/*genetics, Selection, Genetic, Tanzania, Vascular Endothelial Growth Factor Receptor-1/*genetics}, isbn = {1091-6490 (Electronic)0027-8424 (Linking)}, author = {Karumanchi, S. A. and Haig, D.} } @article {509721, title = {Homologous versus antithetic alternation of generations and the origin of sporophytes.}, journal = {Bot Rev}, volume = {74}, year = {2008}, pages = {395}, author = {Haig, D.} } @article {508886, title = {Huddling: brown fat, genomic imprinting and the warm inner glow}, journal = {Curr Biol}, volume = {18}, number = {4}, year = {2008}, note = {

Haig, DavidengEngland2008/02/28 09:00Curr Biol. 2008 Feb 26;18(4):R172-4. doi: 10.1016/j.cub.2007.12.040.

}, month = {Feb 26}, pages = {R172-4}, abstract = {

Heat generated by huddling animals is a public good with a private cost and thus vulnerable to exploitation, as illustrated by recent work on rabbits and penguins. Effects of imprinted genes on brown adipose tissue suggest that non-shivering thermogenesis is an arena for intragenomic conflict.

}, keywords = {*Cooperative Behavior, Adipocytes, Brown/metabolism, Animals, Body Temperature Regulation/genetics/*physiology, Female, Genomic Imprinting/physiology, Male, Maternal Behavior, Mice, Paternal Behavior, Rabbits/*physiology, Spheniscidae/*physiology}, isbn = {0960-9822 (Print)0960-9822 (Linking)}, author = {Haig, D.} } @article {509726, title = {Kinship asymmetries and the divided self.}, journal = {Behv Brain Sci}, volume = {31}, year = {2008}, pages = {271-272}, author = {Haig, D.} } @article {508891, title = {Placental growth hormone-related proteins and prolactin-related proteins}, journal = {Placenta}, volume = {29 Suppl A}, year = {2008}, note = {

Haig, DengReviewEngland2007/11/06 09:00Placenta. 2008 Mar;29 Suppl A:S36-41. Epub 2007 Nov 5.

}, month = {Mar}, pages = {S36-41}, abstract = {

The placentas of ruminants and muroid rodents express prolactin (PRL)-related genes whereas the placentas of anthropoid primates express growth hormone (GH)-related genes. The evolution of placental expression is associated with accelerated evolution of the corresponding pituitary hormone and destabilization of conserved endocrine systems. In particular, placental hormones often evolve novel interactions with new receptors. The adaptive functions of some placental hormones may be revealed only under conditions of physiological stress.

}, keywords = {Animals, Endocrine System/*physiology, Female, Growth Hormone/*physiology, Humans, Placenta/*physiology, Placental Hormones/*physiology, Pregnancy, Prolactin/*physiology}, isbn = {0143-4004 (Print)0143-4004 (Linking)}, author = {Haig, D.} } @article {509456, title = {Reciprocally imprinted genes and the response to selection on one sex}, journal = {Genetics}, volume = {179}, number = {3}, year = {2008}, note = {

Patten, Manus MHaig, DavidengResearch Support, U.S. Gov{\textquoteright}t, Non-P.H.S.2008/06/20 09:00Genetics. 2008 Jul;179(3):1389-94. doi: 10.1534/genetics.107.077651. Epub 2008 Jun 18.

}, month = {Jul}, pages = {1389-94}, abstract = {

We explore the theoretical consequences of limiting selection to males for the evolution of imprinted genes. We find that the efficiency of male-limited selection depends on the pattern of imprinting at an imprinted locus. When selection is strong, the maternally expressed pattern of imprinting allows faster genetic change than the reciprocal, paternally expressed pattern. When selection is relatively weak, the pattern of imprinting that permits a greater rate of genetic response to selection depends on the frequency of the favored allele: the paternally expressed pattern permits faster genetic change than does the maternally expressed pattern at low frequencies of a favored allele; at higher frequencies of a favored allele, however, the maternally expressed pattern is again more conducive to a genetic response. To our knowledge, this is the first theoretical description of a difference between the two reciprocal patterns of imprinting. The selective efficiency bias we identify between the two patterns of imprinting has implications for natural and livestock populations, which we discuss.

}, keywords = {*Selection, Genetic, *Sex Characteristics, Animals, Female, Gene Frequency, Genomic Imprinting/*genetics, Male, Models, Genetic}, isbn = {0016-6731 (Print)0016-6731 (Linking)}, author = {Patten, M. M. and Haig, D.} } @article {508656, title = {Sexual antagonism and the evolution of X chromosome inactivation}, journal = {Evolution}, volume = {62}, number = {8}, year = {2008}, note = {

Engelstadter, JanHaig, DavidengResearch Support, Non-U.S. Gov{\textquoteright}t2008/05/30 09:00Evolution. 2008 Aug;62(8):2097-104. doi: 10.1111/j.1558-5646.2008.00431.x. Epub 2008 May 27.

}, month = {Aug}, pages = {2097-104}, abstract = {

In most female mammals, one of the two X chromosomes is inactivated early in embryogenesis. Expression of most genes on this chromosome is shut down, and the inactive state is maintained throughout life in all somatic cells. It is generally believed that X-inactivation evolved as a means of achieving equal gene expression in males and females (dosage compensation). Following degeneration of genes on the Y chromosome, gene expression on X chromosomes in males and females is upregulated. This results in closer to optimal gene expression in males, but deleterious overexpression in females. In response, selection is proposed to favor inactivation of one of the X chromosomes in females, restoring optimal gene expression. Here, we make a first attempt at shedding light on this intricate process from a population genetic perspective, elucidating the sexually antagonistic selective forces involved. We derive conditions for the process to work and analyze evolutionary stability of the system. The implications of our results are discussed in the light of empirical findings and a recently proposed alternative hypothesis for the evolution of X-inactivation.

}, keywords = {*Gene Expression Regulation, *X Chromosome, *X Chromosome Inactivation, Algorithms, Alleles, Animals, Dosage Compensation, Genetic, Drosophila, Embryonic Development, Female, Heterozygote, Male, Mammals/*genetics/*physiology, Polymorphism, Genetic, Sex Chromosomes}, isbn = {0014-3820 (Print)0014-3820 (Linking)}, author = {Engelstadter, J. and Haig, D.} } @article {509611, title = {Phenotypic heterogeneity is an evolutionarily conserved feature of the endothelium}, journal = {Blood}, volume = {109}, number = {2}, year = {2007}, note = {

Yano, KiichiroGale, DanielMassberg, SteffenCheruvu, Pavan KMonahan-Earley, RitaMorgan, Ellen SHaig, Davidvon Andrian, Ulrich HDvorak, Ann MAird, William Ceng2006/09/23 09:00Blood. 2007 Jan 15;109(2):613-5. Epub 2006 Sep 21.

}, month = {Jan 15}, pages = {613-5}, abstract = {

Mammalian endothelial cells (ECs) display marked phenotypic heterogeneity. Little is known about the evolutionary mechanisms underlying EC heterogeneity. The last common ancestor of hagfish and gnathostomes was also the last common ancestor of all extant vertebrates, which lived some time more than 500 million years ago. Features of ECs that are shared between hagfish and gnathostomes can be inferred to have already been present in this ancestral vertebrate. The goal of this study was to determine whether the hagfish endothelium displays phenotypic heterogeneity. Electron microscopy of the aorta, dermis, heart, and liver revealed ultrastructural heterogeneity of the endothelium. Immunofluorescent studies demonstrated marked differences in lectin binding between vascular beds. Intravital microscopy of the dermis revealed histamine-induced adhesion of leukocytes in capillaries and postcapillary venules, but no such adhesion in arterioles. Together, these data suggest that structural, molecular, and functional heterogeneity of the endothelium evolved as an early feature of this cell lineage.

}, keywords = {Animals, Aorta/ultrastructure, Biological Evolution, Capillaries/cytology, Cell Adhesion, Dermis/blood supply/ultrastructure, Endothelium/*ultrastructure, Hagfishes/*physiology, Heart/anatomy \& histology, Lectins, Leukocytes/cytology, Liver/ultrastructure, Phenotype, Staining and Labeling, Venules/cytology}, isbn = {0006-4971 (Print)0006-4971 (Linking)}, author = {Yano, K. and Gale, D. and Massberg, S. and Cheruvu, P. K. and Monahan-Earley, R. and Morgan, E. S. and Haig, D. and von Andrian, U. H. and Dvorak, A. M. and Aird, W. C.} } @article {509736, title = {Weismann rules! OK? Epigenetics and the Lamarckian temptation.}, journal = {Biol Philos}, volume = {22}, year = {2007}, pages = {415-428}, author = {Haig, D.} } @article {508871, title = {Congenital bilateral absence of the vas deferens and recombination at CFTR}, journal = {Eur J Hum Genet}, volume = {14}, number = {7}, year = {2006}, note = {

Haig, DavidengCommentLetterEngland2006/04/28 09:00Eur J Hum Genet. 2006 Jul;14(7):801; author reply 801. Epub 2006 Apr 26.

}, month = {Jul}, pages = {801; author reply 801}, keywords = {*Recombination, Genetic, Cystic Fibrosis Transmembrane Conductance Regulator/*genetics, Genetic Variation, Humans, Male, Vas Deferens/*abnormalities}, isbn = {1018-4813 (Print)1018-4813 (Linking)}, author = {Haig, D.} } @article {509021, title = {An earlier formulation of the genetic conflict hypothesis of genomic imprinting}, journal = {Nat Genet}, volume = {38}, number = {3}, year = {2006}, note = {

Haig, DavidWestoby, MarkengLetter2006/02/28 09:00Nat Genet. 2006 Mar;38(3):271.

}, month = {Mar}, pages = {271}, keywords = {*Evolution, Molecular, *Genomic Imprinting, *Models, Genetic, Plants/genetics}, isbn = {1061-4036 (Print)1061-4036 (Linking)}, author = {Haig, D. and Westoby, M.} } @article {508881, title = {Intragenomic politics}, journal = {Cytogenet Genome Res}, volume = {113}, number = {1-4}, year = {2006}, note = {

Haig, DengReviewSwitzerland2006/04/01 09:00Cytogenet Genome Res. 2006;113(1-4):68-74.

}, pages = {68-74}, abstract = {

The mammalian genome contains multiple genetic factions with distinct interests in the outcomes of interactions among kin. In the context of an offspring{\textquoteright}s relations with its mother, these factions are proposed to align into two {\textquoteright}parties{\textquoteright}, one favoring increased demand by offspring and the other favoring reduced demand. A possible alignment has inhibitors of demand located on the X chromosome and enhancers of demand located on autosomes, because X-linked loci are maternally derived two-thirds of the time by contrast to autosomal loci which are maternally derived half of the time.

}, keywords = {*Genomics, *Models, Genetic, Animals, Crosses, Genetic, Evolution, Molecular, Female, Genomic Imprinting, Male, Maternal Behavior, Sex Chromosomes}, isbn = {1424-859X (Electronic)1424-8581 (Linking)}, author = {Haig, D.} } @article {508876, title = {Self-imposed silence: parental antagonism and the evolution of X-chromosome inactivation}, journal = {Evolution}, volume = {60}, number = {3}, year = {2006}, note = {

Haig, Davideng2006/04/28 09:00Evolution. 2006 Mar;60(3):440-7.

}, month = {Mar}, pages = {440-7}, abstract = {

A model is proposed for the evolution of X-chromosome inactivation (XCI) in which natural selection initially favors the silencing of paternally derived alleles of X-linked demand inhibitors. The compensatory upregulation of maternally derived alleles establishes a requirement for monoallelic expression in females. For this reason, XCI is self-reinforcing once established. However, inactivation of a particular X chromosome is not. Random XCI (rXCI) is favored over paternal XCI because rXCI reduces the costs of functional hemizygosity in females. Once present, rXCI favors the evolution of locus-by-locus imprinting of X-linked loci, which creates an evolutionary dynamic in which different chromosomes compete to remain active.

}, keywords = {*Biological Evolution, *Models, Biological, *X Chromosome Inactivation, Animals, Dosage Compensation, Genetic, Female, Genes, X-Linked, Male}, isbn = {0014-3820 (Print)0014-3820 (Linking)}, author = {Haig, D.} } @article {509031, title = {Sexual conflict and the alternation of haploid and diploid generations}, journal = {Philos Trans R Soc Lond B Biol Sci}, volume = {361}, number = {1466}, year = {2006}, note = {

Haig, DavidWilczek, AmityengReviewEngland2006/04/15 09:00Philos Trans R Soc Lond B Biol Sci. 2006 Feb 28;361(1466):335-43.

}, month = {Feb 28}, pages = {335-43}, abstract = {

Land plants possess a multicellular diploid stage (sporophyte) that begins development while attached to a multicellular haploid progenitor (gametophyte). Although the closest algal relatives of land plants lack a multicellular sporophyte, they do produce a zygote that grows while attached to the maternal gametophyte. The diploid offspring shares one haploid set of genes with the haploid mother that supplies it with resources and a paternal haploid complement that is not shared with the mother. Sexual conflict can arise within the diploid offspring because the offspring{\textquoteright}s maternal genome will be transmitted in its entirety to all other sexual and asexual offspring that the mother may produce, but the offspring{\textquoteright}s paternally derived genes may be absent from these other offspring. Thus, the selective forces favouring the evolution of genomic imprinting may have been present from the origin of modern land plants. In bryophytes, where gametophytes are long-lived and capable of multiple bouts of asexual and sexual reproduction, we predict strong sexual conflict over allocation to sporophytes. Female gametophytes of pteridophytes produce a single sporophyte and often lack means of asexual reproduction. Therefore, sexual conflict is predicted to be attenuated. Finally, we explore similarities among models of mate choice, offspring choice and segregation distortion.

}, keywords = {*Diploidy, *Haploidy, Bryophyta/*genetics, Chlorophyta/*genetics, Ferns/*genetics, Reproduction/genetics}, isbn = {0962-8436 (Print)0962-8436 (Linking)}, author = {Haig, D. and Wilczek, A.} } @article {509616, title = {Angiogenic factors in the pathogenesis of preeclampsia}, journal = {Curr Top Dev Biol}, volume = {71}, year = {2005}, note = {

Yuan, Hai-TaoHaig, DavidAnanth Karumanchi, SengDK 065997/DK/NIDDK NIH HHS/HL079594/HL/NHLBI NIH HHS/Research Support, N.I.H., ExtramuralReview2005/12/14 09:00Curr Top Dev Biol. 2005;71:297-312.

}, pages = {297-312}, abstract = {

Preeclampsia affects 5-10\% of pregnancies and is responsible for substantial maternal and neonatal morbidity and mortality. It is believed to be a two-stage disease with an initial placental trigger with no maternal symptoms followed by a maternal syndrome characterized by hypertension, proteinuria, and endothelial dysfunction. The first stage is thought to be due to shallow cytotrophoblast invasion of maternal spiral arterioles leading to placental insufficiency. The diseased placenta in turn releases soluble angiogenic factors that induce systemic endothelial dysfunction and clinical preeclampsia during the second stage. This review will discuss the role of circulating angiogenic factors of placental origin as potential mediators of the systemic endothelial dysfunction and the clinical syndrome of preeclampsia and provide an evolutionary explanation for this phenomenon.

}, keywords = {*Angiogenesis Inducing Agents, Angiogenic Proteins/*physiology, Female, Humans, Models, Biological, Placenta/blood supply, Placentation/physiology, Pre-Eclampsia/*etiology, Pregnancy, Pregnancy Proteins/physiology}, isbn = {0070-2153 (Print)0070-2153 (Linking)}, author = {Yuan, H. T. and Haig, D. and Ananth Karumanchi, S.} } @article {508866, title = {The complex history of distal human chromosome 1q}, journal = {Genomics}, volume = {86}, number = {6}, year = {2005}, note = {

Haig, DavidengComparative Study2005/11/19 09:00Genomics. 2005 Dec;86(6):767-70. Epub 2005 Nov 15.

}, month = {Dec}, pages = {767-70}, abstract = {

Human chromosome 1 has been claimed to be a conserved ancestral chromosome of eutherian mammals. However, two small regions from distal 1q (with orthology to mouse chromosome 11) appear to have a different history. These two regions are proposed to have been added to the ancestor of human chromosome 1 as a single block that was subsequently disrupted by a paracentric inversion. The translocation and inversion appear to have occurred at some time after the primate lineage diverged from a common ancestor with rodents. Reconstruction of the history of distal human chromosome 1q is complicated by the "reuse" of breakpoints in different mammalian lineages and by coincidental shared synteny between humans and cats.

}, keywords = {*Chromosome Mapping, *Evolution, Molecular, Chromosomes, Human, Pair 1/*genetics, Computational Biology, Genomics/methods, Humans, Species Specificity, Synteny/genetics, Translocation, Genetic/*genetics}, isbn = {0888-7543 (Print)0888-7543 (Linking)}, author = {Haig, D.} } @article {508576, title = {Divergent mating systems and parental conflict as a barrier to hybridization in flowering plants}, journal = {Am Nat}, volume = {166}, number = {3}, year = {2005}, note = {

Brandvain, YanivHaig, Davideng2005/10/15 09:00Am Nat. 2005 Sep;166(3):330-8. Epub 2005 Jun 28.

}, month = {Sep}, pages = {330-8}, abstract = {

Parental conflicts can lead to antagonistic coevolution of the sexes and of parental genomes. Within a population, the resulting antagonistic effects should balance, but crosses between populations can reveal conflict. Parental conflict is less intense in self-pollinating plants than in outcrossers because outcrossing plants are pollinated by multiple pollen donors unrelated to the seed parent, while a self-pollinating plant is primarily pollinated by one individual (itself). Therefore, in crosses between plants with differing mating systems, outcrossing parents are expected to "overpower" selfing parents. We call this the weak inbreeder/strong outbreeder (WISO) hypothesis. Prezygotically, such overpowering can alter pollination success, and we argue that our hypothesis explains a common pattern of unilateral incompatibility, in which pollen from self-incompatible populations fertilizes ovules of self-compatible individuals but the reciprocal cross fails. A postzygotic manifestation of overpowering is aberrant seed development due to parent-of-origin effects such as genomic imprinting. We evaluate evidence for the WISO hypothesis by reviewing published accounts of crosses between plants of different mating systems. Many, but not all, of such reports support our hypothesis. Since parental conflicts can perturb fertilization and development, such conflicts may strengthen reproductive barriers between populations, contributing to speciation.

}, keywords = {Angiosperms/*physiology, Flowers/physiology, Hybridization, Genetic/*physiology, Pollen/physiology, Reproduction/*physiology, Seeds/physiology}, isbn = {1537-5323 (Electronic)0003-0147 (Linking)}, author = {Brandvain, Y. and Haig, D.} } @article {509576, title = {On the evolutionary stability of Mendelian segregation}, journal = {Genetics}, volume = {170}, number = {3}, year = {2005}, note = {

Ubeda, FranciscoHaig, DavidengResearch Support, Non-U.S. Gov{\textquoteright}t2005/05/25 09:00Genetics. 2005 Jul;170(3):1345-57. Epub 2005 May 23.

}, month = {Jul}, pages = {1345-57}, abstract = {

We present a model of a primary locus subject to viability selection and an unlinked locus that causes sex-specific modification of the segregation ratio at the primary locus. If there is a balanced polymorphism at the primary locus, a population undergoing Mendelian segregation can be invaded by modifier alleles that cause sex-specific biases in the segregation ratio. Even though this effect is particularly strong if reciprocal heterozygotes at the primary locus have distinct viabilities, as might occur with genomic imprinting, it also applies if reciprocal heterozygotes have equal viabilities. The expected outcome of the evolution of sex-specific segregation distorters is all-and-none segregation schemes in which one allele at the primary locus undergoes complete drive in spermatogenesis and the other allele undergoes complete drive in oogenesis. All-and-none segregation results in a population in which all individuals are maximally fit heterozygotes. Unlinked modifiers that alter the segregation ratio are unable to invade such a population. These results raise questions about the reasons for the ubiquity of Mendelian segregation.

}, keywords = {*Evolution, Molecular, *Genetics, Population, *Models, Genetic, Chromosome Segregation/*genetics, Genetic Load, Meiosis/*genetics, Sex Factors}, isbn = {0016-6731 (Print)0016-6731 (Linking)}, author = {Ubeda, F. and Haig, D.} } @article {509431, title = {Phylogenetic analyses of the core antenna domain: investigating the origin of photosystem I}, journal = {J Mol Evol}, volume = {60}, number = {2}, year = {2005}, note = {

Mix, Lucas JHaig, DavidCavanaugh, Colleen MengResearch Support, U.S. Gov{\textquoteright}t, Non-P.H.S.2005/03/24 09:00J Mol Evol. 2005 Feb;60(2):153-63.

}, month = {Feb}, pages = {153-63}, abstract = {

Phototrophy, the conversion of light to biochemical energy, occurs throughout the Bacteria and plants, however, debate continues over how different phototrophic mechanisms and the bacteria that contain them are related. There are two types of phototrophic mechanisms in the Bacteria: reaction center type 1 (RC1) has core and core antenna domains that are parts of a single polypeptide, whereas reaction center type 2 (RC2) is composed of short core proteins without antenna domains. In cyanobacteria, RC2 is associated with separate core antenna proteins that are homologous to the core antenna domains of RC1. We reconstructed evolutionary relationships among phototrophic mechanisms based on a phylogeny of core antenna domains/proteins. Core antenna domains of 46 polypeptides were aligned, including the RC1 core proteins of heliobacteria, green sulfur bacteria, and photosystem I (PSI) of cyanobacteria and plastids, plus core antenna proteins of photosystem II (PSII) from cyanobacteria and plastids. Maximum likelihood, parsimony, and neighbor joining methods all supported a single phylogeny in which PSII core antenna proteins (PsbC, PsbB) arose within the cyanobacteria from duplications of the RC1-associated core antenna domains and accessory antenna proteins (IsiA, PcbA, PcbC) arose from duplications of PsbB. The data indicate an evolutionary history of RC1 in which an initially homodimeric reaction center was vertically transmitted to green sulfur bacteria, heliobacteria, and an ancestor of cyanobacteria. A heterodimeric RC1 (=PSI) then arose within the cyanobacterial lineage. In this scenario, the current diversity of core antenna domains/proteins is explained without a need to invoke horizontal transfer.

}, keywords = {Amino Acid Sequence, Bacteria/classification/*genetics/*metabolism, Evolution, Molecular, Molecular Sequence Data, Photobiology, Photosystem I Protein Complex/chemistry/*genetics/metabolism, Phylogeny, Protein Structure, Tertiary, Sequence Homology, Amino Acid}, isbn = {0022-2844 (Print)0022-2844 (Linking)}, author = {Mix, L. J. and Haig, D. and Cavanaugh, C. M.} } @article {509371, title = {Reinforcement of pre-zygotic isolation and karyotype evolution in Agrodiaetus butterflies}, journal = {Nature}, volume = {436}, number = {7049}, year = {2005}, note = {

Lukhtanov, Vladimir AKandul, Nikolai PPlotkin, Joshua BDantchenko, Alexander VHaig, DavidPierce, Naomi EengComparative StudyResearch Support, Non-U.S. Gov{\textquoteright}tResearch Support, U.S. Gov{\textquoteright}t, Non-P.H.S.England2005/07/22 09:00Nature. 2005 Jul 21;436(7049):385-9.

}, month = {Jul 21}, pages = {385-9}, abstract = {

The reinforcement model of evolution argues that natural selection enhances pre-zygotic isolation between divergent populations or species by selecting against unfit hybrids or costly interspecific matings. Reinforcement is distinguished from other models that consider the formation of reproductive isolation to be a by-product of divergent evolution. Although theory has shown that reinforcement is a possible mechanism that can lead to speciation, empirical evidence has been sufficiently scarce to raise doubts about the importance of reinforcement in nature. Agrodiaetus butterflies (Lepidoptera: Lycaenidae) exhibit unusual variability in chromosome number. Whereas their genitalia and other morphological characteristics are largely uniform, different species vary considerably in male wing colour, and provide a model system to study the role of reinforcement in speciation. Using comparative phylogenetic methods, we show that the sympatric distribution of 15 relatively young sister taxa of Agrodiaetus strongly correlates with differences in male wing colour, and that this pattern is most likely the result of reinforcement. We find little evidence supporting sympatric speciation: rather, in Agrodiaetus, karyotypic changes accumulate gradually in allopatry, prompting reinforcement when karyotypically divergent races come into contact.

}, keywords = {*Evolution, Molecular, *Selection, Genetic, Animals, Butterflies/anatomy \& histology/classification/*genetics/*physiology, Chromosomes/genetics, Color, Female, Karyotyping, Male, Models, Biological, Phylogeny, Pigmentation/physiology, Reproduction/physiology, Species Specificity, Time Factors, Wing/anatomy \& histology/physiology, Zygote/physiology}, isbn = {1476-4687 (Electronic)0028-0836 (Linking)}, author = {Lukhtanov, V. A. and Kandul, N. P. and Plotkin, JB and Dantchenko, A. V. and Haig, D. and Pierce, N. E.} } @article {510476, title = {Deciphering the genomic palimpsest.}, journal = {Curr Opin Gen Dev}, volume = {14}, year = {2004}, pages = {599-602}, author = {Haig, D. and Henikoff, S.} } @article {508846, title = {The (dual) origin of epigenetics}, journal = {Cold Spring Harb Symp Quant Biol}, volume = {69}, year = {2004}, note = {

Haig, DengHistorical ArticleReview2005/08/25 09:00Cold Spring Harb Symp Quant Biol. 2004;69:67-70.

}, pages = {67-70}, keywords = {*Epigenesis, Genetic, Animals, Genetics/history, History, 20th Century, Terminology as Topic}, isbn = {0091-7451 (Print)0091-7451 (Linking)}, author = {Haig, D.} } @article {508861, title = {Evolutionary conflicts in pregnancy and calcium metabolism--a review}, journal = {Placenta}, volume = {25 Suppl A}, year = {2004}, note = {

Haig, DengReviewEngland2004/03/23 05:00Placenta. 2004 Apr;25 Suppl A:S10-5.

}, month = {Apr}, pages = {S10-5}, abstract = {

The maternal-fetal unit contains three distinct haplotypes at each locus: the maternally derived fetal haplotype (MDFH) that is shared by the mother and fetus, the paternally derived fetal haplotype (PDFH), and the non-inherited maternal haplotype (NIMH). The evolutionary forces acting on these haplotypes are distinct. The NIMH is absent from the offspring and could benefit from early abortion if this enhances the probability of the mother conceiving again and producing an offspring that inherits the NIMH. This raises the possibility that some forms of recurrent spontaneous abortion may be caused by non-inherited haplotypes. Such {\textquoteright}selfish{\textquoteright} behaviour would be opposed by other components of the maternal genome. Natural selection acting on genes expressed in fetuses (or their placentae) favours greater maternal investment in the fetus than does natural selection acting on genes expressed in mothers. Furthermore, in the presence of genomic imprinting, the PDFH favours greater levels of investment in the fetus than does the MDFH. These conflicts are illustrated using the example of maternal-fetal conflicts over the supply of calcium. Inactivation of the paternal copy of GNAS in proximal renal tubule is interpreted as a measure to maintain fetal bone mineralization in times of calcium stress at the expense of the maternal skeleton.

}, keywords = {*Evolution, Molecular, *Paternity, Adult, Calcium/*metabolism, Female, Genomic Imprinting/*genetics, Humans, Male, Pregnancy/*genetics/*metabolism}, isbn = {0143-4004 (Print)0143-4004 (Linking)}, author = {Haig, D.} } @article {508851, title = {Genomic imprinting and kinship: how good is the evidence?}, journal = {Annu Rev Genet}, volume = {38}, year = {2004}, note = {

Haig, DavidengReview2004/12/01 09:00Annu Rev Genet. 2004;38:553-85.

}, pages = {553-85}, abstract = {

The kinship theory of genomic imprinting proposes that parent-specific gene expression evolves at a locus because a gene{\textquoteright}s level of expression in one individual has fitness effects on other individuals who have different probabilities of carrying the maternal and paternal alleles of the individual in which the gene is expressed. Therefore, natural selection favors different levels of expression depending on an allele{\textquoteright}s sex-of-origin in the previous generation. This review considers the strength of evidence in support of this hypothesis for imprinted genes in four "clusters," associated with the imprinted loci Igf2, Igf2r, callipyge, and Gnas. The clusters associated with Igf2 and Igf2r both contain paternally expressed transcripts that act as enhancers of prenatal growth and maternally expressed transcripts that act as inhibitors of prenatal growth. This is consistent with predictions of the kinship theory. However, the clusters also contain imprinted genes whose phenotypes as yet remain unexplained by the theory. The principal effects of imprinted genes in the callipyge and Gnas clusters appear to involve lipid and energy metabolism. The kinship theory predicts that maternally expressed transcripts will favor higher levels of nonshivering thermogenesis (NST) in brown adipose tissue (BAT) of animals that huddle for warmth as offspring. The phenotypes of reciprocal heterozygotes for Gnas knockouts provide provisional support for this hypothesis, as does some evidence from other imprinted genes (albeit more tentatively). The diverse effects of imprinted genes on the development of white adipose tissue (WAT) have so far defied a unifying hypothesis in terms of the kinship theory.

}, keywords = {*Genomic Imprinting, *Models, Genetic, Alleles, Animals, Beckwith-Wiedemann Syndrome/genetics, Evolution, Molecular, GTP-Binding Protein alpha Subunits, Gs/genetics, Humans, Insulin-Like Growth Factor II/genetics, Mice, Mice, Knockout, Multigene Family, Phenotype, Sheep, Uniparental Disomy}, isbn = {0066-4197 (Print)0066-4197 (Linking)}, author = {Haig, D.} } @article {508856, title = {The inexorable rise of gender and the decline of sex: social change in academic titles, 1945-2001}, journal = {Arch Sex Behav}, volume = {33}, number = {2}, year = {2004}, note = {

Haig, DavidengHistorical Article2004/05/18 05:00Arch Sex Behav. 2004 Apr;33(2):87-96.

}, month = {Apr}, pages = {87-96}, abstract = {

More than 30 million titles of "academic" articles, from the years 1945-2001, were surveyed for occurrences of the words sex and gender. At the beginning of this period, uses of gender were much rarer than uses of sex, and often used in the sense of a grammatical category. By the end of this period, uses of gender outnumbered uses of sex in the social sciences, arts, and humanities. Within the natural sciences, there was now more than 1 use of gender for every 2 uses of sex. The beginnings of this change in usage can be traced to Money{\textquoteright}s introduction of the concept of "gender role" in 1955 (J. Money, 1955). However, the major expansion in the use of gender followed its adoption by feminists to distinguish the social and cultural aspects of differences between men and women (gender) from biological differences (sex). Since then, the use of gender has tended to expand to encompass the biological, and a sex/gender distinction is now only fitfully observed.

}, keywords = {*Gender Identity, *Sex, *Social Perception, *Terminology as Topic, Cultural Characteristics, Female, History, 20th Century, Humans, Journalism, Medical/*history, Male, Sexual Behavior, Time Factors, United States}, isbn = {0004-0002 (Print)0004-0002 (Linking)}, author = {Haig, D.} } @article {509331, title = {Phylogeny of Agrodiaetus Hubner 1822 (Lepidoptera: Lycaenidae) inferred from mtDNA sequences of COI and COII and nuclear sequences of EF1-alpha: karyotype diversification and species radiation}, journal = {Syst Biol}, volume = {53}, number = {2}, year = {2004}, note = {

Kandul, Nikolai PLukhtanov, Vladimir ADantchenko, Alexander VColeman, James W SSekercioglu, Cagan HHaig, DavidPierce, Naomi EengComparative StudyResearch Support, Non-U.S. Gov{\textquoteright}tResearch Support, U.S. Gov{\textquoteright}t, Non-P.H.S.England2004/06/19 05:00Syst Biol. 2004 Apr;53(2):278-98.

}, month = {Apr}, pages = {278-98}, abstract = {

Butterflies in the large Palearctic genus Agrodiaetus (Lepidoptera: Lycaenidae) are extremely uniform and exhibit few distinguishing morphological characters. However, these insects are distinctive in one respect: as a group they possess among the greatest interspecific karyotype diversity in the animal kingdom, with chromosome numbers (n) ranging from 10 to 125. The monophyly of Agrodiaetus and its systematic position relative to other groups within the section Polyommatus have been controversial. Characters from the mitochondrial genes for cytochrome oxidases I and II and from the nuclear gene for elongation factor 1 alpha were used to reconstruct the phylogeny of Agrodiaetus using maximum parsimony and Bayesian phylogenetic methods. Ninety-one individuals, encompassing most of the taxonomic diversity of Agrodiaetus, and representatives of 14 related genera were included in this analysis. Our data indicate that Agrodiaetus is monophyletic. Representatives of the genus Polyommatus (sensu stricto) are the closest relatives. The sequences of the Agrodiaetus taxa in this analysis are tentatively arranged into 12 clades, only 1 of which corresponds to a species group traditionally recognized in Agrodiaetus. Heterogeneous substitution rates across a recovered topology were homogenized with a nonparametric rate-smoothing algorithm before the application of a molecular clock. Two published estimates of substitution rates dated the origin of Agrodiaetus between 2.51 and 3.85 million years ago. During this time, there was heterogeneity in the rate and direction of karyotype evolution among lineages within the genus. Karyotype instability has evolved independently three times in the section Polyommatus, within the lineages Agrodiaetus, Lysandra, and Plebicula. Rapid karyotype diversification may have played a significant role in the radiation of the genus Agrodiaetus.

}, keywords = {*Evolution, Molecular, *Phylogeny, Animals, Base Sequence, Bayes Theorem, Butterflies/*genetics, Chromosomes/*genetics, DNA Primers, DNA, Mitochondrial/genetics, Karyotyping, Models, Genetic, Molecular Sequence Data, Peptide Elongation Factor 1/genetics, Sequence Analysis, DNA, Time Factors}, isbn = {1063-5157 (Print)1063-5157 (Linking)}, author = {Kandul, N. P. and Lukhtanov, V. A. and Dantchenko, A. V. and Coleman, J. W. and Sekercioglu, C. H. and Haig, D. and Pierce, N. E.} } @article {509571, title = {Sex-specific meiotic drive and selection at an imprinted locus}, journal = {Genetics}, volume = {167}, number = {4}, year = {2004}, note = {

Ubeda, FranciscoHaig, DavidengResearch Support, Non-U.S. Gov{\textquoteright}t2004/09/03 05:00Genetics. 2004 Aug;167(4):2083-95.

}, month = {Aug}, pages = {2083-95}, abstract = {

We present a one-locus model that breaks two symmetries of Mendelian genetics. Whereas symmetry of transmission is breached by allowing sex-specific segregation distortion, symmetry of expression is breached by allowing genomic imprinting. Simple conditions for the existence of at least one polymorphic stable equilibrium are provided. In general, population mean fitness is not maximized at polymorphic equilibria. However, mean fitness at a polymorphic equilibrium with segregation distortion may be higher than mean fitness at the corresponding equilibrium with Mendelian segregation if one (or both) of the heterozygote classes has higher fitness than both homozygote classes. In this case, mean fitness is maximized by complete, but opposite, drive in the two sexes. We undertook an extensive numerical analysis of the parameter space, finding, for the first time in this class of models, parameter sets yielding two stable polymorphic equilibria. Multiple equilibria exist both with and without genomic imprinting, although they occurred in a greater proportion of parameter sets with genomic imprinting.

}, keywords = {*Genomic Imprinting, *Polymorphism, Genetic, *Selection, Genetic, Chromosome Mapping, Diploidy, Female, Humans, Male, Models, Genetic, Models, Statistical, Sex Characteristics}, isbn = {0016-6731 (Print)0016-6731 (Linking)}, author = {Ubeda, F. and Haig, D.} } @article {510486, title = {The amoral roots of morality.}, journal = {Lahey Clinic Medical Ethics}, volume = {10}, year = {2003}, pages = {10-11}, author = {Haig, D.} } @article {510496, title = {The science that dare not speak its name.}, journal = {Quarterly Review of BIology}, volume = {78}, year = {2003}, pages = {327-335}, author = {Haig, D.} } @article {508841, title = {Behavioural genetics: Family matters}, journal = {Nature}, volume = {421}, number = {6922}, year = {2003}, note = {

Haig, DavidengCommentNewsResearch Support, Non-U.S. Gov{\textquoteright}tEngland2003/01/31 04:00Nature. 2003 Jan 30;421(6922):491-2.

}, month = {Jan 30}, pages = {491-2}, keywords = {*Behavior, Animal, *Maternal Behavior, *Models, Genetic, *Paternal Behavior, Animals, Birth Weight, Conflict (Psychology), Crosses, Genetic, Extrachromosomal Inheritance/genetics, Female, Genomic Imprinting/*genetics, Genotype, Litter Size/genetics, Male, Mice, Mice, Inbred C57BL, Mice, Inbred CBA, Models, Animal, Species Specificity}, isbn = {0028-0836 (Print)0028-0836 (Linking)}, author = {Haig, D.} } @article {509566, title = {Dividing the child}, journal = {Genetica}, volume = {117}, number = {1}, year = {2003}, note = {

Ubeda, FranciscoHaig, DavidengResearch Support, Non-U.S. Gov{\textquoteright}tNetherlands2003/03/27 05:00Genetica. 2003 Jan;117(1):103-10.

}, month = {Jan}, pages = {103-10}, abstract = {

The evolution of genomic imprinting is viewed as a problem of economic optimization that is analyzed using the tools of evolutionary game theory. We specifically consider genetic conflicts over the allocation of maternal resources between present and future offspring. Five sets of genes, with the same interests within sets but distinct interests between sets, are considered as agents: maternal alleles (Mater), paternal alleles (Pater), unimprinted offspring alleles (Filius), and imprinted offspring alleles of maternal and paternal origin (Matris and Patris). Fitness functions are derived for each agent and the parameter space in which there is conflict defined. Three potential conflicts are considered: between mother and offspring (Mater v.s. Filius); between alleles of maternal and paternal origin within offspring (Matris v.s. Patris) and between mothers and the paternally derived alleles of offspring (Mater v.s. Patris).

}, keywords = {*Evolution, Molecular, *Models, Genetic, Alleles, Game Theory, Gene Expression/*genetics, Genomic Imprinting/*genetics}, isbn = {0016-6707 (Print)0016-6707 (Linking)}, author = {Ubeda, F. and Haig, D.} } @article {509601, title = {Inbreeding, maternal care and genomic imprinting}, journal = {J Theor Biol}, volume = {221}, number = {4}, year = {2003}, note = {

Wilkins, Jon FHaig, DavidengResearch Support, Non-U.S. Gov{\textquoteright}tEngland2003/04/26 05:00J Theor Biol. 2003 Apr 21;221(4):559-64.

}, month = {Apr 21}, pages = {559-64}, abstract = {

Inactivation of expression of the paternal allele at two maternally silent imprinted loci has recently been reported to diminish the quality of care that female mice lavish on their offspring. This suggests that there can be disagreement between the maternally and paternally derived genomes of mothers over how much care for offspring is appropriate, with the paternally derived genome favoring greater care. The reason for such disagreement is not obvious because the maternally and paternally derived alleles at a locus have equal probabilities of being transmitted to each of the mother{\textquoteright}s ova and, therefore, would appear to have equal interests in a mother{\textquoteright}s offspring. However, if a female mates with a related male, her two alleles may have different probabilities of being present in the sperm that fertilize her ova. Natural selection can favor silencing of the maternally derived allele at a locus that enhances the quality of maternal care if the average patrilineal relatedness between a female and her mates decreases more rapidly than the average matrilineal relatedness. Just such an asymmetrical decrease in relatedness over time would be expected in a structured population in which patrilineal inbreeding is more common than matrilineal inbreeding.

}, keywords = {*Genomic Imprinting, *Inbreeding, *Models, Genetic, Animals, Female, Learning, Maternal Behavior/*physiology, Mice, Phylogeny, Selection, Genetic}, isbn = {0022-5193 (Print)0022-5193 (Linking)}, author = {Wilkins, J. F. and Haig, D.} } @article {509761, title = {On intrapersonal reciprocity.}, journal = {Evol Human Behav}, volume = {24}, year = {2003}, pages = {418-425}, author = {Haig, D.} } @article {508836, title = {Meditations on birth weight: is it better to reduce the variance or increase the mean?}, journal = {Epidemiology}, volume = {14}, number = {4}, year = {2003}, note = {

Haig, DavidengCambridge, Mass.2003/07/05 05:00Epidemiology. 2003 Jul;14(4):490-2.

}, month = {Jul}, pages = {490-2}, abstract = {

A conceptual model is presented here in which the birth weight distribution is decomposed into a distribution of target weights and a distribution of perturbations from the target. The target weight is the adaptive goal of fetal development. In the simplest model, perinatal mortality is independent of variation in target weight and determined solely by the magnitude of the perturbation of birth weight from the target. In this model, mortality risk is concentrated in the tails of the birth weight distribution. A difference between populations in their distributions of target weights will be associated with a corresponding shift in their curves of weight-specific risk, without any difference between the populations in overall risk. In this model, risk would be reduced by decreasing the variance of the distribution of perturbations. The model is discussed in the context of the so-called "paradoxes of low birth weight."

}, keywords = {*Birth Weight, *Infant Mortality, *Models, Theoretical, *Statistics as Topic, Humans, Infant, Newborn, Risk Assessment}, isbn = {1044-3983 (Print)1044-3983 (Linking)}, author = {Haig, D.} } @article {509026, title = {Prader-Willi syndrome and the evolution of human childhood}, journal = {Am J Hum Biol}, volume = {15}, number = {3}, year = {2003}, note = {

Haig, DavidWharton, Roberteng2003/04/22 05:00Am J Hum Biol. 2003 May-Jun;15(3):320-9.

}, month = {May-Jun}, pages = {320-9}, abstract = {

The kinship theory of genomic imprinting predicts that imprinted genes have effects on asymmetric kin (relatives with different degrees of matrilineal and patrilineal relatedness). The most important interaction with such a relative is a child{\textquoteright}s interaction with its mother. Therefore, the study of imprinted genes and their phenotypic effects promises to provide insights into the evolution of mother-child relations. Prader-Willi syndrome (PWS) is caused by the absence of expression of genes at 15q11-q13 that are normally expressed only when paternally derived. The kinship theory predicts that children with PWS will fail to express behaviors that have increased mothers{\textquoteright} costs of child-rearing. Our analysis focuses on aspects of the PWS phenotype that affect appetite and feeding. Immediately after birth, children with PWS have little appetite and are usually unable to suckle, but at some stage (usually within the first 2 years) they develop a voracious appetite and an obsession with food. We conjecture that this change in appetite reflects evolutionary forces associated with weaning. Immediately after birth, when a child is completely dependent on the breast, poor appetite reduced maternal costs. However, once a child was able to consume supplemental foods, maternal costs would have been reduced by children with increased, nonfastidious appetites.

}, keywords = {*Biological Evolution, *Mother-Child Relations, Appetite/physiology, Breast Feeding, Child Development, Chromosomes, Human, Pair 15, Energy Metabolism, Humans, Infant, Infant Food, Infant, Newborn, Phenotype, Prader-Willi Syndrome/embryology/genetics/*physiopathology, Puberty}, isbn = {1042-0533 (Print)1042-0533 (Linking)}, author = {Haig, D. and Wharton, R.} } @article {508506, title = {Sostrup statement on low birthweight}, journal = {Int J Epidemiol}, volume = {32}, number = {5}, year = {2003}, note = {

Adams, MelissaAndersen, Anne-Marie NyboAndersen, Per KraghHaig, DavidHenriksen, Tine BrinkHertz-Picciotto, IrvaLie, Rolv TerjeOlsen, JornSkjaerven, RolvWilcox, AllenengConsensus Development ConferenceReviewEngland2003/10/16 05:00Int J Epidemiol. 2003 Oct;32(5):884-5.

}, month = {Oct}, pages = {884-5}, keywords = {*Birth Weight, *Infant, Low Birth Weight, Epidemiologic Methods, Health Status Indicators, Humans, Infant Mortality, Infant, Newborn}, isbn = {0300-5771 (Print)0300-5771 (Linking)}, author = {Adams, M. and Andersen, A. M. and Andersen, P. K. and Haig, D. and Henriksen, T. B. and Hertz-Picciotto, I. and Lie, R. T. and Olsen, J. and Skjaerven, R. and Wilcox, A.} } @article {509596, title = {What good is genomic imprinting: the function of parent-specific gene expression}, journal = {Nat Rev Genet}, volume = {4}, number = {5}, year = {2003}, note = {

Wilkins, Jon FHaig, DavidengReviewEngland2003/05/03 05:00Nat Rev Genet. 2003 May;4(5):359-68.

}, month = {May}, pages = {359-68}, abstract = {

Parent-specific gene expression (genomic imprinting) is an evolutionary puzzle because it forgoes an important advantage of diploidy--protection against the effects of deleterious recessive mutations. Three hypotheses claim to have found a countervailing selective advantage of parent-specific expression. Imprinting is proposed to have evolved because it enhances evolvability in a changing environment, protects females against the ravages of invasive trophoblast, or because natural selection acts differently on genes of maternal and paternal origin in interactions among kin. The last hypothesis has received the most extensive theoretical development and seems the best supported by the properties of known imprinted genes. However, the hypothesis is yet to provide a compelling explanation for many examples of imprinting.

}, keywords = {*Selection, Genetic, Animals, Evolution, Molecular, Female, Gene Expression Regulation, Gene Expression/*physiology, Genomic Imprinting/*genetics, Humans, Male, Models, Genetic, Parents, Sex Factors}, isbn = {1471-0056 (Print)1471-0056 (Linking)}, author = {Wilkins, J. F. and Haig, D.} } @article {509766, title = {The Inclusive fitness dynamics of genomic imprinting}, journal = {Selection}, volume = {2}, year = {2002}, pages = {103-118}, author = {Greenwood-Lee, J.M. and Taylor, P.D. and Haig, D.} } @article {509591, title = {Parental modifiers, antisense transcripts and loss of imprinting}, journal = {Proc Biol Sci}, volume = {269}, number = {1502}, year = {2002}, note = {

Wilkins, Jon FHaig, DavidengResearch Support, Non-U.S. Gov{\textquoteright}tEngland2002/09/28 04:00Proc Biol Sci. 2002 Sep 7;269(1502):1841-6.

}, month = {Sep 7}, pages = {1841-6}, abstract = {

The kinship theory of genomic imprinting has explained parent-specific gene expression as the outcome of an evolutionary conflict between the two alleles at a diploid locus of an offspring over how much to demand from parents. Previous models have predicted that maternally derived (madumnal) alleles will be silent at demand-enhancing loci, while paternally derived (padumnal) alleles will be silent at demand-suppressing loci, but these models have not considered the evolution of trans-acting modifiers that are expressed in parents and influence imprinted expression in offspring. We show that such modifiers will sometimes be selected to reactivate the silent padumnal allele at a demand-suppressing locus but will not be selected to reactivate the silent madumnal allele at a demand-enhancing locus. Therefore, imprinting of demand-suppressing loci is predicted to be less evolutionarily stable than imprinting of demand-enhancing loci.

}, keywords = {*Genomic Imprinting, Alleles, Animals, Biological Evolution, DNA Methylation, DNA, Antisense/genetics, Female, Gene Silencing, Male, Models, Genetic, Mutation, Transcription, Genetic}, isbn = {0962-8452 (Print)0962-8452 (Linking)}, author = {Wilkins, J. F. and Haig, D.} } @article {509586, title = {Genomic imprinting of two antagonistic loci}, journal = {Proc Biol Sci}, volume = {268}, number = {1479}, year = {2001}, note = {

Wilkins, J FHaig, DengResearch Support, U.S. Gov{\textquoteright}t, P.H.S.England2001/09/21 10:00Proc Biol Sci. 2001 Sep 22;268(1479):1861-7.

}, month = {Sep 22}, pages = {1861-7}, abstract = {

We present a model that considers the coevolution of genomic imprinting at a growth factor locus and an antagonistic growth suppressor locus. With respect to the two loci considered independently, our model makes the familiar predictions that an imprinted growth factor locus will only be expressed from the paternally derived allele and an imprinted growth suppressor locus only from the maternally derived allele. In addition, our coevolutionary model allows us to make predictions regarding the sequence of evolutionary events necessary for generating such a system. We conclude that imprinting at the growth factor locus preceded the evolution of growth suppressor function at the second locus, which in turn preceded imprinting at that locus. We then discuss the consistency of these predictions with currently available comparative data on the insulin-like growth factor 2 insulin-like growth factor 2 receptor system of mammals.

}, keywords = {*Genomic Imprinting, *Models, Genetic, Animals, Humans, Insulin-Like Growth Factor II/*genetics, Receptor, IGF Type 2/*genetics}, isbn = {0962-8452 (Print)0962-8452 (Linking)}, author = {Wilkins, J. F. and Haig, D.} } @article {510501, title = {Of sex and gender.}, journal = {Nat Genet}, volume = {25}, year = {2000}, pages = {373}, author = {Haig, D.} } @article {508831, title = {Genomic imprinting, sex-biased dispersal, and social behavior}, journal = {Ann NY Acad Sci}, volume = {907}, year = {2000}, note = {

Haig, Deng2000/05/20 09:00Ann N Y Acad Sci. 2000 Apr;907:149-63.

}, month = {Apr}, pages = {149-63}, abstract = {

Some genes carry a record of the sex of the gene{\textquoteright}s carrier in the previous generation that influences the gene{\textquoteright}s expression in this generation. This additional information can result in intragenomic conflicts between an individual{\textquoteright}s maternally and paternally derived alleles over behaviors that affect relatives with whom the individual has different degrees of maternal and paternal relatedness. Asymmetries of relatedness can arise because of sex-biased dispersal. For example, if females remain in their natal group and males disperse, female members of a group will all be matrilineal relatives, but may have unrelated fathers. Sex-linked inheritance creates an evolutionary bias in favor of social groups that trace descent through the homogametic sex. This bias has a positive and negative aspect. The positive aspect is increased relatedness among siblings of the homogametic sex. The negative aspect is the lack of sex-linked relatedness between parents and offspring of the heterogametic sex.

}, keywords = {*Genomic Imprinting, *Social Behavior, Female, Humans, Male, Sex Factors}, isbn = {0077-8923 (Print)0077-8923 (Linking)}, author = {Haig, D.} } @article {509036, title = {Genomic imprinting, sibling solidairity and the logic of collective action}, journal = {Philos Trans R Soc Lond B Biol Sci}, volume = {355}, number = {1403}, year = {2000}, note = {

Haig, DWilkins, J FengEngland2000/12/29 11:00Philos Trans R Soc Lond B Biol Sci. 2000 Nov 29;355(1403):1593-7.

}, month = {Nov 29}, pages = {1593-7}, abstract = {

Genomic imprinting has been proposed to evolve when a gene{\textquoteright}s expression has fitness consequences for individuals with different coefficients of matrilineal and patrilineal relatedness, especially in the context of competition between offspring for maternal resources. Previous models have focused on pre-emptive hierarchies, where conflict arises with respect to resource allocation between present and future offspring. Here we present a model in which imprinting arises from scramble competition within litters. The model predicts paternal-specific expression of a gene that increases an offspring{\textquoteright}s fractional share of resources but reduces the size of the resource pool, and maternal-specific expression of a gene with opposite effects. These predictions parallel the observation in economic models that individuals tend to underprovide public goods, and that the magnitude of this shortfall increases with the number of individuals in the group. Maternally derived alleles are more willing than their paternally derived counterparts to contribute to public goods because they have a smaller effective group size.

}, keywords = {*Genomic Imprinting, Animals, Behavior, Animal, Competitive Behavior, Models, Genetic}, isbn = {0962-8436 (Print)0962-8436 (Linking)}, author = {Haig, D. and Wilkins, J. F.} } @article {508826, title = {Of sex and gender}, journal = {Nat Genet}, volume = {25}, number = {4}, year = {2000}, note = {

Haig, DengLetter2000/08/10 11:00Nat Genet. 2000 Aug;25(4):373.

}, month = {Aug}, pages = {373}, keywords = {*Sex, *Terminology as Topic, Animals, Female, Humans, Male, Periodicals as Topic}, isbn = {1061-4036 (Print)1061-4036 (Linking)}, author = {Haig, D.} } @article {509006, title = {William Hamilton (1936-2000)}, journal = {Science}, volume = {287}, number = {5462}, year = {2000}, note = {

Haig, DPierce, N EWilson, E OengBiographyHistorical ArticlePortraitsNew York, N.Y.2000/04/15Science. 2000 Mar 31;287(5462):2438.

}, month = {Mar 31}, pages = {2438}, keywords = {Biological Evolution, Biology/history, England, History, 20th Century, United States}, isbn = {0036-8075 (Print)0036-8075 (Linking)}, author = {Haig, D. and Pierce, N. E. and Wilson, E. O.} } @article {508811, title = {A brief history of human autosomes}, journal = {Philos Trans R Soc Lond B Biol Sci}, volume = {354}, number = {1388}, year = {1999}, note = {

Haig, DengComparative StudyReviewENGLAND1999/10/09Philos Trans R Soc Lond B Biol Sci. 1999 Aug 29;354(1388):1447-70.

}, month = {Aug 29}, pages = {1447-70}, abstract = {

Comparative gene mapping and chromosome painting permit the tentative reconstruction of ancestral karyotypes. The modern human karyotype is proposed to differ from that of the most recent common ancestor of catarrhine primates by two major rearrangements. The first was the fission of an ancestral chromosome to produce the homologues of human chromosomes 14 and 15. This fission occurred before the divergence of gibbons from humans and other apes. The second was the fusion of two ancestral chromosomes to form human chromosome 2. This fusion occurred after the divergence of humans and chimpanzees. Moving further back in time, homologues of human chromosomes 3 and 21 were formed by the fission of an ancestral linkage group that combined loci of both human chromosomes, whereas homologues of human chromosomes 12 and 22 were formed by a reciprocal translocation between two ancestral chromosomes. Both events occurred at some time after our most recent common ancestor with lemurs. Less direct evidence suggests that the short and long arms of human chromosomes 8, 16 and 19 were unlinked in this ancestor. Finally, the most recent common ancestor of primates and artiodactyls is proposed to have possessed a chromosome that combined loci from human chromosomes 4 and 8p, a chromosome that combined loci from human chromosomes 16q and 19q, and a chromosome that combined loci from human chromosomes 2p and 20.

}, keywords = {*Evolution, Molecular, *Models, Genetic, Animals, Chromosome Mapping/methods, Chromosomes, Human/*genetics, Genetics, Medical/*methods, Humans, Karyotyping, Phylogeny, Primates/*genetics, Telomere/genetics}, isbn = {0962-8436 (Print)0962-8436 (Linking)}, author = {Haig, D.} } @article {508816, title = {Genetic conflicts and the private life of Peromyscus polionotus}, journal = {Nat Genet}, volume = {22}, number = {2}, year = {1999}, note = {

Haig, DengCommentLetter1999/06/16 10:00Nat Genet. 1999 Jun;22(2):131.

}, month = {Jun}, pages = {131}, keywords = {*Genomic Imprinting, *Sexual Behavior, Animal, Animals, Female, Male, Peromyscus/*genetics/psychology}, isbn = {1061-4036 (Print)1061-4036 (Linking)}, author = {Haig, D.} } @article {508821, title = {Multiple paternity and genomic imprinting}, journal = {Genetics}, volume = {151}, number = {3}, year = {1999}, note = {

Haig, DengCommentLetter1999/05/08Genetics. 1999 Mar;151(3):1229-31.

}, month = {Mar}, pages = {1229-31}, keywords = {*Genomic Imprinting, *Models, Statistical, *Paternity, Evolution, Molecular, Gene Expression, Models, Genetic}, isbn = {0016-6731 (Print)0016-6731 (Linking)}, author = {Haig, D.} } @article {508996, title = {A quantitative measure of error minimization in the genetic code}, journal = {J Mol Evol}, volume = {49}, number = {5}, year = {1999}, note = {

HaigHurstEng1999/11/07J Mol Evol. 1999 Nov;49(5):708.

}, month = {Nov}, pages = {708}, isbn = {1432-1432 (Electronic)0022-2844 (Linking)}, author = {Haig, D. and Hurst, L. D.} } @article {508806, title = {What is a marmoset?}, journal = {Am J Primatol}, volume = {49}, number = {4}, year = {1999}, note = {

Haig, DengReview1999/11/30 09:00Am J Primatol. 1999 Dec;49(4):285-96.

}, month = {Dec}, pages = {285-96}, abstract = {

Callitrichid primates typically give birth to twin offspring that are somatic chimeras of cells derived from two products of conception. Each individual is thus the phenotype of two sibling genotypes, one of which may be more closely related to the germ line of the individual{\textquoteright}s parents than to the individual{\textquoteright}s own germ line. Chimerism could therefore help to explain the evolution of alloparental care and social suppression of reproduction in callitrichids. Placental chimerism may also have important implications for understanding kin interactions within the womb: on one side of the coin, the intimate juxtaposition of genotypes provides unique opportunities for antagonistic interactions between embryos; on the other side, chimerism could facilitate cooperation between sibling genotypes.

}, keywords = {*Pregnancy, Animal, *Pregnancy, Multiple, Animals, Bone Marrow/physiology, Callithrix/*genetics/physiology, Chimera/*genetics/physiology, Female, Fetus/physiology, Game Theory, Genotype, Male, Phenotype, Placenta/physiology, Pregnancy, Sexual Behavior, Animal, Twins}, isbn = {0275-2565 (Print)0275-2565 (Linking)}, author = {Haig, D.} } @article {508796, title = {All in the family}, journal = {Trends Ecol Evol}, volume = {13}, number = {11}, year = {1998}, note = {

Haig, DengEngland1998/11/01 00:00Trends Ecol Evol. 1998 Nov 1;13(11):468.

}, month = {Nov 1}, pages = {468}, abstract = {

The Evolution of Sibling Rivalry by D.W. Mock and G.A. Parker Oxford University Press, 1998. $120.00 hbk, $55.00 pbk (xiii +464 pages) ISBN 0 19 857743 5/0 19 857744 3.

}, isbn = {0169-5347 (Print)0169-5347 (Linking)}, author = {Haig, D.} } @article {508801, title = {Mother{\textquoteright}s boy or daddy{\textquoteright}s girl? Sex determination in Hymenoptera}, journal = {Trends Ecol Evol}, volume = {13}, number = {10}, year = {1998}, note = {

Haig, DengEngland1998/10/01 00:00Trends Ecol Evol. 1998 Oct 1;13(10):380-1.

}, month = {Oct 1}, pages = {380-1}, isbn = {0169-5347 (Print)0169-5347 (Linking)}, author = {Haig, D.} } @article {510506, title = {"When sense and antisense combine" (verse)}, journal = {Antisense \& Nucleic Acid Drug Dev}, volume = {7}, year = {1997}, pages = {1}, author = {Haig, D.} } @article {508781, title = {Maternal-fetal interactions and MHC polymorphism}, journal = {J Reprod Immunol}, volume = {35}, number = {2}, year = {1997}, note = {

Haig, DengIRELAND1998/01/09J Reprod Immunol. 1997 Nov 15;35(2):101-9.

}, month = {Nov 15}, pages = {101-9}, abstract = {

Two models of maternal-fetal interactions are discussed. In the first, offspring are advantaged if they possess an allele absent in their mother. Polymorphism is maintained because rare alleles have an advantage when present in males. In the second, offspring are disadvantaged if they lack an allele present in their mother. Polymorphism is maintained because rare alleles have an advantage when present in females. Both classes of model are associated with a deficiency of homozygous genotypes. If the artificial assumption of symmetrical selection is relaxed, the second class of model (gestational drive) could account for the otherwise inexplicable absence of MHC polymorphism in some species.

}, keywords = {*Major Histocompatibility Complex, *Models, Genetic, *Polymorphism, Genetic, Alleles, Animals, Female, Humans, Maternal-Fetal Exchange, Pregnancy}, isbn = {0165-0378 (Print)0165-0378 (Linking)}, author = {Haig, D.} } @article {508786, title = {Parental antagonism, relatedness asymmetries, and genomic imprinting}, journal = {Proc Biol Sci}, volume = {264}, number = {1388}, year = {1997}, note = {

Haig, DengENGLAND1997/12/24Proc Biol Sci. 1997 Nov 22;264(1388):1657-62.

}, month = {Nov 22}, pages = {1657-62}, abstract = {

The theory of inclusive fitness can be modified to consider separate coefficients of relatedness for an individual{\textquoteright}s maternal and paternal alleles. A gene is said to have parentally antagonistic effects if it has an inclusive fitness benefit when maternally derived, but an inclusive fitness cost when paternally derived (or vice versa). Parental antagonism favours the evolution of alleles that are expressed only when maternally derived or only when paternally derived (genomic imprinting).

}, keywords = {*Genomic Imprinting, *Models, Genetic, Animals, Evolution, Molecular, Female, Insulin-Like Growth Factor II/genetics, Male, Mathematical Computing, Mice, Receptor, IGF Type 2/genetics, Sex Factors}, isbn = {0962-8452 (Print)0962-8452 (Linking)}, author = {Haig, D.} } @article {508791, title = {William Turner{\textquoteright}s lectures on the comparative anatomy of the placenta}, journal = {Placenta}, volume = {18}, number = {4}, year = {1997}, note = {

Haig, DengBiographyHistorical ArticleENGLAND1997/05/01Placenta. 1997 May;18(4):371-4.

}, month = {May}, pages = {371-4}, keywords = {Anatomy, Comparative/*history, Female, History, 19th Century, History, 20th Century, Humans, Placenta/*anatomy \& histology, Pregnancy}, isbn = {0143-4004 (Print)0143-4004 (Linking)}, author = {Haig, D.} } @article {508771, title = {Altercation of generations: genetic conflicts of pregnancy}, journal = {Am J Reprod Immunol}, volume = {35}, number = {3}, year = {1996}, note = {

Haig, DengReviewDENMARKNew York, N.Y. : 19891996/03/01Am J Reprod Immunol. 1996 Mar;35(3):226-32.

}, month = {Mar}, pages = {226-32}, abstract = {

Pregnancy is traditionally viewed as a harmonious collaboration between mother and fetus. From this perspective, viviparity poses a series of problems that maternal and fetal genes work together to solve and the many complications of pregnancy are interpreted as evidence of the malfunctioning of an evolved system or of the failure of natural selection to achieve an adaptive goal. This view fails to recognize aspects of genetic conflict that lie at the heart of gestation. At least three interrelated sources of conflict can be identified: (i) conflict between genes expressed in the mother and genes expressed in the fetus/placenta (parent-offspring conflict); (ii) conflict between maternally-derived and paternally-derived genes within the fetal genome (genomic imprinting); and (iii) conflict between maternal genes that recognize themselves in offspring and the rest of the maternal genome (gestational drive).

}, keywords = {Animals, Biological Evolution, Embryonic and Fetal Development/*genetics, Female, Genomic Imprinting/genetics, Humans, Maternal-Fetal Exchange/*genetics, Pregnancy, Animal/*genetics, Pregnancy/*genetics}, isbn = {1046-7408 (Print)1046-7408 (Linking)}, author = {Haig, D.} } @article {508766, title = {Do imprinted genes have few and small introns?}, journal = {Bioessays}, volume = {18}, number = {5}, year = {1996}, note = {

Haig, DengReviewENGLAND1996/05/01Bioessays. 1996 May;18(5):351-3.

}, month = {May}, pages = {351-3}, abstract = {

A gene is described as imprinted if its pattern of expression depends on whether it passed the previous generation in a male or female germ line. A recent paper reports that imprinted genes have fewer and smaller introns than a control set of genes. The differences are striking but their interpretation is unclear. The loss of introns after a gene becomes imprinted is not sufficient to explain why imprinted genes have fewer introns than average, because related unimprinted genes also have few introns. Similarly, small introns appear to be a property of chromosomal region rather than of imprinting status itself, because neighboring unimprinted genes also have small introns.

}, keywords = {*Chromosome Mapping, *Genomic Imprinting, *Introns, Animals, Biological Evolution, Chromosomes, Human, Female, Genome, Human, Humans, Male, Mice, Models, Genetic, Selection, Genetic}, isbn = {0265-9247 (Print)0265-9247 (Linking)}, author = {Haig, D.} } @article {508761, title = {Gestational drive and the green-bearded placenta}, journal = {Proc Natl Acad Sci USA}, volume = {93}, number = {13}, year = {1996}, note = {

Haig, DengResearch Support, Non-U.S. Gov{\textquoteright}t1996/06/25Proc Natl Acad Sci U S A. 1996 Jun 25;93(13):6547-51.

}, month = {Jun 25}, pages = {6547-51}, abstract = {

A "green beard" refers to a gene, or group of genes, that is able to recognize itself in other individuals and direct benefits to these individuals. Green-beard effects have been dismissed as implausible by authors who have implicitly assumed sophisticated mechanisms of perception and complex behavioral responses. However, many simple mechanisms for genes to "recognize" themselves exist at the maternal-fetal interface of viviparous organisms. Homophilic cell adhesion molecules, for example, are able to interact with copies of themselves on other cells. Thus, the necessary components of a green-beard effect -- feature, recognition, and response -- can be different aspects of the phenotype of a single gene. Other green-beard effects could involve coalitions of genes at closely linked loci. In fact, any form of epistasis between a locus expressed in a mother and a closely linked locus expressed in the fetus has the property of "self-recognition." Green-beard effects have many formal similarities to systems of meiotic drive and, like them, can be a source of intragenomic conflict.

}, keywords = {Cell Adhesion/genetics, Female, Genetic Diseases, Inborn/genetics, Genetic Linkage, Genomic Imprinting, Heterozygote, Humans, Maternal-Fetal Exchange/genetics, Meiosis/genetics, Placenta/*physiology, Pregnancy Maintenance, Pregnancy/*genetics}, isbn = {0027-8424 (Print)0027-8424 (Linking)}, author = {Haig, D.} } @article {508776, title = {The pea and the coconut: seed size in safe sites}, journal = {Trends Ecol Evol}, volume = {11}, number = {1}, year = {1996}, note = {

Haig, DengEngland1996/01/01 00:00Trends Ecol Evol. 1996;11(1):1-2.

}, pages = {1-2}, isbn = {0169-5347 (Print)0169-5347 (Linking)}, author = {Haig, D.} } @article {509281, title = {Sociobiology{\textquoteright}s Successes}, journal = {Science}, volume = {274}, number = {5285}, year = {1996}, note = {

Hrdy, S BRodman, PCharnov, E LSeger, JHawkes, KEmlen, S TFoster, S AGowaty, P AHaig, DHauser, MJacobs, L FSmuts, B BengNew York, N.Y.1996/10/11 00:00Science. 1996 Oct 11;274(5285):162-3.

}, month = {Oct 11}, pages = {162-3}, isbn = {0036-8075 (Print)0036-8075 (Linking)}, author = {Hrdy, S. B. and Rodman, P. and Charnov, E. L. and Seger, J. and Hawkes, K. and Emlen, S. T. and Foster, S. A. and Gowaty, P. A. and Haig, D. and Hauser, M. and Jacobs, L. F. and Smuts, B. B.} } @article {510511, title = {Prenatal power plays.}, journal = {Nat Hist}, volume = {104}, year = {1995}, pages = {39}, author = {Haig, D.} } @article {508756, title = {Whitridge Williams{\textquoteright} obstetrics}, journal = {Am J Obstet Gynecol}, volume = {173}, number = {4}, year = {1995}, note = {

Haig, DengBiographyHistorical ArticleLetter1995/10/01Am J Obstet Gynecol. 1995 Oct;173(4):1351.

}, month = {Oct}, pages = {1351}, keywords = {Ethics, Medical/*history, History, 20th Century, Obstetrics/*history, United States}, isbn = {0002-9378 (Print)0002-9378 (Linking)}, author = {Haig, D.} } @article {508741, title = {Cohabitation and pregnancy-induced hypertension}, journal = {Lancet}, volume = {344}, number = {8937}, year = {1994}, note = {

Haig, DengCommentLetterENGLAND1994/12/10Lancet. 1994 Dec 10;344(8937):1633-4; author reply 1634-5.

}, month = {Dec 10}, pages = {1633-4; author reply 1634-5}, keywords = {*Genomic Imprinting, *Spermatozoa, Coitus, Female, Humans, Hypertension/*etiology, Male, Pregnancy, Pregnancy Complications, Cardiovascular/*etiology, Time Factors}, isbn = {0140-6736 (Print)0140-6736 (Linking)}, author = {Haig, D.} } @article {508751, title = {Is human insulin imprinted?}, journal = {Nat Genet}, volume = {7}, number = {1}, year = {1994}, note = {

Haig, DengCommentComparative StudyLetter1994/05/01Nat Genet. 1994 May;7(1):10.

}, month = {May}, pages = {10}, keywords = {Adult, Alleles, Animals, Diabetes Mellitus, Type 1/congenital/genetics, Female, Fetal Growth Retardation/genetics, Humans, Infant, Newborn, Insulin/deficiency/*genetics, Male, Mice/genetics, Parents, Phenotype}, isbn = {1061-4036 (Print)1061-4036 (Linking)}, author = {Haig, D.} } @article {508746, title = {Refusing the ovarian time bomb}, journal = {Trends Genet}, volume = {10}, number = {10}, year = {1994}, note = {

Haig, DengCommentLetterENGLAND1994/10/01Trends Genet. 1994 Oct;10(10):346-7; author reply 348-9.

}, month = {Oct}, pages = {346-7; author reply 348-9}, keywords = {*Genomic Imprinting, *Ovary, Animals, Biological Evolution, DNA Replication, Female, Humans, Ovarian Neoplasms/genetics, Teratoma/genetics, Trophoblasts}, isbn = {0168-9525 (Print)0168-9525 (Linking)}, author = {Haig, D.} } @article {510516, title = {Genomic imprinting, human chorionic gonadotropin, and triploidy.}, journal = {Prenatal Diag}, volume = {13}, year = {1993}, pages = {151}, author = {Haig, D.} } @article {508731, title = {Alternatives to meiosis: the unusual genetics of red algae, microsporidia, and others}, journal = {J Theor Biol}, volume = {163}, number = {1}, year = {1993}, note = {

Haig, DengResearch Support, Non-U.S. Gov{\textquoteright}tENGLAND1993/07/07J Theor Biol. 1993 Jul 7;163(1):15-31.

}, month = {Jul 7}, pages = {15-31}, abstract = {

At a reductional division, the two alleles at a heterozygous locus segregate into different daughter nuclei. Reductional divisions are therefore vulnerable to genetic elements that cause one cell to attack its sister. This danger can be circumvented by creating uncertainty about when reduction occurs. In conventional meiosis, this is achieved by a sequence of two divisions with crossing over. Either the first or the second division can be reductional for most loci. In some red algae, reduction appears to be spread over more than two divisions. The novel reduction sequence of microsporidia creates maximal uncertainty about the time of reduction in two divisions without crossing over.

}, keywords = {*Meiosis, Alleles, Animals, Chromosomes, Microsporida/*genetics, Models, Genetic, Rhodophyta/*genetics}, isbn = {0022-5193 (Print)0022-5193 (Linking)}, author = {Haig, D.} } @article {508726, title = {Genetic conflicts in human pregnancy}, journal = {Q Rev Biol}, volume = {68}, number = {4}, year = {1993}, note = {

Haig, DengResearch Support, Non-U.S. Gov{\textquoteright}tReview1993/12/01Q Rev Biol. 1993 Dec;68(4):495-532.

}, month = {Dec}, pages = {495-532}, abstract = {

Pregnancy has commonly been viewed as a cooperative interaction between a mother and her fetus. The effects of natural selection on genes expressed in fetuses, however, may be opposed by the effects of natural selection on genes expressed in mothers. In this sense, a genetic conflict can be said to exist between maternal and fetal genes. Fetal genes will be selected to increase the transfer of nutrients to their fetus, and maternal genes will be selected to limit transfers in excess of some maternal optimum. Thus a process of evolutionary escalation is predicted in which fetal actions are opposed by maternal countermeasures. The phenomenon of genomic imprinting means that a similar conflict exists within fetal cells between genes that are expressed when maternally derived, and genes that are expressed when paternally derived. During implantation, fetally derived cells (trophoblast) invade the maternal endometrium and remodel the endometrial spiral arteries into low-resistance vessels that are unable to constrict. This invasion has three consequences. First, the fetus gains direct access to its mother{\textquoteright}s arterial blood. Therefore, a mother cannot reduce the nutrient content of blood reaching the placenta without reducing the nutrient supply to her own tissues. Second, the volume of blood reaching the placenta becomes largely independent of control by the local maternal vasculature. Third, the placenta is able to release hormones and other substances directly into the maternal circulation. Placental hormones, including human chorionic gonadotropin (hCG) and human placental lactogen (hPL), are predicted to manipulate maternal physiology for fetal benefit. For example, hPL is proposed to act on maternal prolactin receptors to increase maternal resistance to insulin. If unopposed, the effect of hPL would be to maintain higher blood glucose levels for longer periods after meals. This action, however, is countered by increased maternal production of insulin. Gestational diabetes develops if the mother is unable to mount an adequate response to fetal manipulation. Similarly, fetal genes are predicted to enhance the flow of maternal blood through the placenta by increasing maternal blood pressure. Preeclampsia can be interpreted as an attempt by a poorly nourished fetus to increase its supply of nutrients by increasing the resistance of its mother{\textquoteright}s peripheral circulation.

}, keywords = {Chorionic Gonadotropin/physiology, Embryo Implantation, Embryonic and Fetal Development, Female, Growth Hormone/physiology, Humans, Maternal-Fetal Exchange/genetics, Pre-Eclampsia/etiology, Pregnancy Maintenance, Pregnancy/*genetics/immunology/physiology, Prolactin/physiology}, isbn = {0033-5770 (Print)0033-5770 (Linking)}, author = {Haig, D.} } @article {508736, title = {Genomic imprinting, human chorionic gonadotropin, and triploidy}, journal = {Prenat Diagn}, volume = {13}, number = {2}, year = {1993}, note = {

Haig, DengLetterENGLAND1993/02/01Prenat Diagn. 1993 Feb;13(2):151.

}, month = {Feb}, pages = {151}, keywords = {*Polyploidy, Animals, Chorionic Gonadotropin/*blood, Female, Horses, Humans, Perissodactyla, Pregnancy/*blood}, isbn = {0197-3851 (Print)0197-3851 (Linking)}, author = {Haig, D.} } @article {508721, title = {Intragenomic conflict and the evolution of eusociality}, journal = {J Theor Biol}, volume = {156}, number = {3}, year = {1992}, note = {

Haig, DengLetterENGLAND1992/06/07J Theor Biol. 1992 Jun 7;156(3):401-3.

}, month = {Jun 7}, pages = {401-3}, keywords = {*Biological Evolution, *Models, Genetic, *Social Behavior, Animals, Female, Male}, isbn = {0022-5193 (Print)0022-5193 (Linking)}, author = {Haig, D.} } @article {508981, title = {Genetic scrambling as a defence against meiotic drive}, journal = {J Theor Biol}, volume = {153}, number = {4}, year = {1991}, note = {

Haig, DGrafen, AengENGLAND1991/12/21J Theor Biol. 1991 Dec 21;153(4):531-58.

}, month = {Dec 21}, pages = {531-58}, abstract = {

Genetic recombination has important consequences, including the familiar rules of Mendelian genetics. Here we present a new argument for the evolutionary function of recombination based on the hypothesis that meiotic drive systems continually arise to threaten the fairness of meiosis. These drive systems act at the expense of the fitness of the organism as a whole for the benefit of the genes involved. We show that genes increasing crossing over are favoured, in the process of breaking up drive systems and reducing the fitness loss to organisms.

}, keywords = {*Models, Genetic, Alleles, Biological Evolution, Meiosis/*genetics, Recombination, Genetic/*physiology}, isbn = {0022-5193 (Print)0022-5193 (Linking)}, author = {Haig, D. and Grafen, A.} } @article {508986, title = {Genomic imprinting and the strange case of the insulin-like growth factor II receptor}, journal = {Cell}, volume = {64}, number = {6}, year = {1991}, note = {

Haig, DGraham, CengReview1991/03/22Cell. 1991 Mar 22;64(6):1045-6.

}, month = {Mar 22}, pages = {1045-6}, keywords = {Animals, Fathers, Female, Gene Expression Regulation/genetics, Heterozygote, Insulin-Like Growth Factor II/*metabolism, Male, Mannosephosphates/metabolism, Mothers, Receptor, IGF Type 2, Receptors, Cell Surface/*genetics, Receptors, Somatomedin}, isbn = {0092-8674 (Print)0092-8674 (Linking)}, author = {Haig, D. and Graham, C.} } @article {509436, title = {Genomic imprinting in mammalian development: a parental tug-of-war}, journal = {Trends Genet}, volume = {7}, number = {2}, year = {1991}, note = {

Moore, THaig, DengResearch Support, Non-U.S. Gov{\textquoteright}tReviewENGLAND1991/02/01Trends Genet. 1991 Feb;7(2):45-9.

}, month = {Feb}, pages = {45-9}, abstract = {

Genomic imprinting in mammals is increasingly being implicated in developmental and pathological processes, but without a clear understanding of its function in normal development. We believe that imprinting has evolved in mammals because of the conflicting interests of maternal and paternal genes in relation to the transfer of nutrients from the mother to her offspring. We present an hypothesis that accounts for many of the observed effects of imprinting in mammals and relates them to similar observations in plants. This hypothesis has implications for studies of X-chromosome inactivation and a range of human diseases.

}, keywords = {*Biological Evolution, *Gene Expression, Animals, Embryonic and Fetal Development/genetics, Humans, X Chromosome/*metabolism}, isbn = {0168-9525 (Print)0168-9525 (Linking)}, author = {Moore, T. and Haig, D.} } @article {509291, title = {Prion infection}, journal = {Nature}, volume = {351}, number = {6321}, year = {1991}, note = {

Hurst, L DHaig, DengLetterENGLAND1991/05/02Nature. 1991 May 2;351(6321):21.

}, month = {May 2}, pages = {21}, keywords = {Animals, Chaperonins, Heat-Shock Proteins/*metabolism, Prions/*physiology, Proteins/*metabolism, Viral Proteins/*metabolism, Virus Replication}, isbn = {0028-0836 (Print)0028-0836 (Linking)}, author = {Hurst, L. D. and Haig, D.} } @article {508991, title = {A quantitative measure of error minimization in the genetic code}, journal = {J Mol Evol}, volume = {33}, number = {5}, year = {1991}, note = {

Haig, DHurst, L DengResearch Support, Non-U.S. Gov{\textquoteright}t1991/11/01J Mol Evol. 1991 Nov;33(5):412-7.

}, month = {Nov}, pages = {412-7}, abstract = {

We have calculated the average effect of changing a codon by a single base for all possible single-base changes in the genetic code and for changes in the first, second, and third codon positions separately. Such values were calculated for an amino acid{\textquoteright}s polar requirement, hydropathy, molecular volume, and isoelectric point. For each attribute the average effect of single-base changes was also calculated for a large number of randomly generated codes that retained the same level of redundancy as the natural code. Amino acids whose codons differed by a single base in the first and third codon positions were very similar with respect to polar requirement and hydropathy. The major differences between amino acids were specified by the second codon position. Codons with U in the second position are hydrophobic, whereas most codons with A in the second position are hydrophilic. This accounts for the observation of complementary hydropathy. Single-base changes in the natural code had a smaller average effect on polar requirement than all but 0.02\% of random codes. This result is most easily explained by selection to minimize deleterious effects of translation errors during the early evolution of the code.

}, keywords = {*Amino Acids, *Genetic Code, *Models, Genetic, Codon, Protein Conformation, Proteins/chemistry/genetics}, isbn = {0022-2844 (Print)0022-2844 (Linking)}, author = {Haig, D. and Hurst, L. D.} } @article {510646, title = {Parent-specific gene expression and the triploid endosperm.}, journal = {Am Nat}, volume = {134}, year = {1989}, pages = {147-155}, author = {Haig, D. and Westoby, M.} } @article {510641, title = {Selective forces in the emergence of the seed habit.}, journal = {Biol J Linn Soc}, volume = {38}, year = {1989}, pages = {215-238}, author = {Haig, D. and Westoby, M.} } @article {508716, title = {Seed size and adaptation}, journal = {Trends Ecol Evol}, volume = {4}, number = {5}, year = {1989}, note = {

Haig, DengLetterEngland1989/05/01 00:00Trends Ecol Evol. 1989 May;4(5):145. doi: 10.1016/0169-5347(89)90214-0.

}, month = {May}, pages = {145}, isbn = {0169-5347 (Print)0169-5347 (Linking)}, author = {Haig, D.} } @article {510651, title = {On limits to seed production.}, journal = {Am Nat}, volume = {131}, year = {1988}, pages = {757-759}, author = {Haig, D. and Westoby, M.} } @article {510661, title = {A model for the origin of heterospory.}, journal = {J Theor Biol}, volume = {134}, year = {1988}, pages = {257-272}, author = {Haig, D. and Westoby, M.} } @article {510656, title = {Sex expression in homosporous ferns: an evolutionary perspective.}, journal = {Evol Trends Plants}, volume = {2}, year = {1988}, pages = {111-119}, author = {Haig, D. and Westoby, M.} } @article {508711, title = {Kin conflict in seed plants}, journal = {Trends Ecol Evol}, volume = {2}, number = {11}, year = {1987}, note = {

Haig, DengEngland1987/11/01 00:00Trends Ecol Evol. 1987 Nov;2(11):337-40. doi: 10.1016/0169-5347(87)90110-8.

}, month = {Nov}, pages = {337-40}, abstract = {

Kin selection theory proposes that individuals value the reproductive success of relatives at a rate determined by their probability of shared alleles. The theory predicts when the interests of relatives are in accord and when they conflict. Though kin selection arguments have revolutionized the study of animal behavior, they have only recently been applied to plants. Kin selection has already been claimed to explain the formation of endosperm by double fertilization. This is the character that distinguishes angiosperms from gymnosperms. Plant life cycles involve interactions among kinds of relatives not encountered in animals. These interactions should be a fertile field for new applications of theory and the testing of ideas originally developed elsewhere.

}, isbn = {0169-5347 (Print)0169-5347 (Linking)}, author = {Haig, D.} } @article {510666, title = {Conflicts among megaspores.}, journal = {J Theor Biol}, volume = {123}, year = {1986}, pages = {471-480}, author = {Haig, D.} }