# Publications

1999
Haig D. Multiple paternity and genomic imprinting. Genetics. 1999;151 :1229-31.
Haig D, Hurst LD. A quantitative measure of error minimization in the genetic code. J Mol Evol. 1999;49 :708.
Haig D. What is a marmoset?. Am J Primatol. 1999;49 :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's parents than to the individual'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.

1998
Haig D. All in the family. Trends Ecol Evol. 1998;13 :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.

Haig D. Mother's boy or daddy's girl? Sex determination in Hymenoptera. Trends Ecol Evol. 1998;13 :380-1.
1997
Haig D. "When sense and antisense combine" (verse). Antisense & Nucleic Acid Drug Dev. 1997;7 :1.
Haig D. Maternal-fetal interactions and MHC polymorphism. J Reprod Immunol. 1997;35 :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.

Haig D. Parental antagonism, relatedness asymmetries, and genomic imprinting. Proc Biol Sci. 1997;264 :1657-62.Abstract

The theory of inclusive fitness can be modified to consider separate coefficients of relatedness for an individual'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).

Haig D. William Turner's lectures on the comparative anatomy of the placenta. Placenta. 1997;18 :371-4.
1996
Haig D. Altercation of generations: genetic conflicts of pregnancy. Am J Reprod Immunol. 1996;35 :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).

Haig D. Do imprinted genes have few and small introns?. Bioessays. 1996;18 :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.

Haig D. Gestational drive and the green-bearded placenta. Proc Natl Acad Sci USA. 1996;93 :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.

Haig D. The pea and the coconut: seed size in safe sites. Trends Ecol Evol. 1996;11 :1-2.
Hrdy SB, Rodman P, Charnov EL, Seger J, Hawkes K, Emlen ST, Foster SA, Gowaty PA, Haig D, Hauser M, et al. Sociobiology's Successes. Science. 1996;274 :162-3.
1995
Haig D. Prenatal power plays. Nat Hist. 1995;104 (12) :39.
Haig D. Whitridge Williams' obstetrics. Am J Obstet Gynecol. 1995;173 :1351.
1994
Haig D. Cohabitation and pregnancy-induced hypertension. Lancet. 1994;344 :1633-4; author reply 1634-5.
Haig D. Is human insulin imprinted?. Nat Genet. 1994;7 :10.
Haig D. Refusing the ovarian time bomb. Trends Genet. 1994;10 :346-7; author reply 348-9.