Common misconceptions of the 'parental conflict' 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.
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'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' 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' health and could be associated with substantial detrimental effects.
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.
Variation in body composition is a popular obsession. The culturally 'ideal' 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.
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.
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.
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.
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' lactational amenorrhea, thus delaying the birth of a younger sib and enhancing infant survival.
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.
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.
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.
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 ‘ultimate cause’ be abandoned as ambiguous.
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.
