In the Light of Evolution Volume V: Cooperation and Conflict (2011) / Chapter Skim
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12 Genomic Imprinting and the Evolutionary Psychology of Human Kinship--DAVID HAIG
12 Genomic Imprinting and the Evolutionary Psychology of Human Kinship--DAVID HAIG
Pages 253-274
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From page 253... ...
. Effects of imprinted genes are not predicted in interactions with nonrelatives or with individuals who are equally related to the actor's maternally and paternally derived genes (unless a gene also has pleiotropic effects on fitness of asymmetric kin)
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From page 254... ...
ASYMMETRIES OF RELATEDNESS Consider an imprinted locus at which the established allele is silent when paternally derived but expressed at level x > 0 when maternally derived. This pattern of expression is an evolutionarily stable strategy (ESS)
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From page 255... ...
specifies that extra x reduces patrilineal inclusive fitness. This condition maintains silence of paternally derived alleles.
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From page 256... ...
. The ESS for a locus at which the established allele is silent when maternally derived but expressed at level z > 0 when paternally derived is obtained by substitution of z for x and reciprocal substitution of m for p throughout the above analysis.
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From page 257... ...
An actor can treat another individual as belonging to an innate category without recognizing that a category exists or recognizing particular individuals as members of the category. As a simple example, h ormones secreted into the maternal circulation by a fetus affect another individual who necessarily carries copies of the maternally derived alleles of the fetus (Haig, 1996)
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From page 258... ...
. To the extent that this evocation is suc cessful, culture thereby changes the coefficients of relatedness associated with an innate category in ongoing natural selection.
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From page 259... ...
Her future offspring are potentially also the offspring's father 's future offspring. However, when a mother changes partner, her continued reproduction expends limited maternal i nvestment on maternal halfsibs, who are unrelated rivals from the perspective of paternally derived genes of existing offspring.
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From page 260... ...
. Infants with PWS exhibit poor suck, weak cry, and excessive sleepi ness, suggesting paternally expressed genes from 15q11–13 promote suckling, strength of cry, and wakefulness (all phenotypes that are expected to enhance maternal costs)
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From page 261... ...
Paternal-specific expression of imprinted genes is expected to benefit self at the expense of uterine sibs, whereas maternal-specific expression is expected to benefit uterine sibs at a cost to self. Two factors in human evolution have probably had opposing effects on the intensity of conflict between genes of maternal and paternal origin over relations with uterine sibs.
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From page 262... ...
Paternal halfsibs are patrikin, but it is unclear whether we have evolved innate dispositions that are specific for this category of kin. Relations with paternal halfsibs are usually less intimate than relations with maternal halfsibs because a father's contact with his offspring becomes attenuated once his sexual relations with their mother ends, especially if he has offspring with another woman.
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From page 263... ...
A key unanswered question is whether this cultural distinction is reinforced by innate dispositions that distinguish "mother's kin" from "father's kin," or whether the two kinds of kin are lumped together in a single instinctive category with asymmetries of relatedness determined by social context. The recognition of particular individuals as belonging to particu lar categories of kin enables discrimination among members of social groups on the basis of degree of relatedness (nepotism)
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From page 264... ...
By further extension, a mother is kith of the paternally derived genes of her own offspring. These genes have an interest in her well-being to the extent that the offspring's individual fitness depends on continued investment by a healthy mother.
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From page 265... ...
, because genes of maternal origin in the child have no direct interest in the father 's continued reproduc tion, whereas genes of paternal origin have no direct interest in the mother's continued reproduction. Therefore, genes of paternal origin are expected to promote reduced cooperation with mothers after divorce, either expressed as increased demands for maternal resources, increased competition with maternal halfsibs, or reduced expression of helpful behaviors.
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From page 266... ...
Ego's genes of paternal origin have less of an interest in the younger sib's welfare than ego's genes of maternal origin. There fore, this scenario predicts maternal-specific expression of accelerators of puberty and paternal-specific expression of decelerators of puberty.
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From page 267... ...
Partner change causes a decrease in p2, thus discounting the cost of competition with the younger sib, or discounting the ben efit of helping raise the younger sib, for genes of paternal origin. In the another-mouth-to-feed scenario, reduced relatedness to younger sibs
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From page 268... ...
However, the accel eration of puberty due to increased z may favor enhanced production of x from alleles of maternal origin as a countermeasure. By contrast, in the helper-at-the-nest scenario, reduced relatedness to younger sibs directly favors increased production of x from alleles of paternal origin t o hasten the onset of puberty.
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From page 269... ...
In the second instance, genes that predispose men to short-term relationships would become statistically associated with genes of paternal origin that predispose daughters to mature early, and thus avoid sacrificing personal reproduction for the benefit of maternal
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From page 270... ...
Therefore, the helper-at-the-nest hypothesis predicts earlier menarche for daughters with fewer younger sibs and later menarche for elder daughters in larger families. A British study found correlations broadly consistent with these predictions: Menarche was delayed in girls from larger families, but girls born later in a family of a given size had earlier menarche (Dann and Roberts, 1993)
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From page 271... ...
However, evidence from the effects of imprinted genes on pubertal progression is not readily compatible with the helper-at-the-nest hypothesis. PWS and Silver-Russell syndrome are caused by the absence of paternally expressed genes or increased dosage of maternally expressed genes.
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From page 272... ...
Adolescence is a life-history transition in which the expression of imprinted genes may have significant effects within the brain. The maternal and paternal genomes of the adolescent agree about individual fitness but may disagree over how much individual fitness should be killed for investment in indirect fitness via kin.
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From page 273... ...
For most categories of kin, relatedness differs for genes of maternal and paternal origin. The inclusive fitness of maternal and paternal alleles will be maximized by different allocations of fitness among kin, creating the potential for conflicting goals within individual organisms and a deep-seated biological ambivalence in relations among kin.
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From page 274... ...
274 / David Haig Maternal and paternal genes have a common interest in the effec tive functioning of the individual actor, but phenotypes that are deter mined by agents with different fitness functions are not expected to show the degree of integration and physiological efficiency one would expect of a phenotype determined by agents with identical interests. Perhaps such internal conflicts can partially account for inefficiencies of mental function and a high frequency of pathology in human social interactions.
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