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Parental antagonism, relatedness asymmetries, and genomic imprinting (1997)

by David Haig
Venue:Proc R Soc Lond B
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The elements of a scientific theory of self-deception

by Robert Trivers - Annals of the New York Academy of Sciences 907:114–31. [AP, HJL, aWvH] Trivers, R. (2009) Deceit and self-deception. In: Mind the , 2000
"... ABSTRACT: An evolutionary theory of self-deception—the active misrepresentation of reality to the conscious mind—suggests that there may be multiple sources of self-deception in our own species, with important interactions between them. Self-deception (along with internal conflict and fragmentation) ..."
Abstract - Cited by 51 (0 self) - Add to MetaCart
ABSTRACT: An evolutionary theory of self-deception—the active misrepresentation of reality to the conscious mind—suggests that there may be multiple sources of self-deception in our own species, with important interactions between them. Self-deception (along with internal conflict and fragmentation) may serve to improve deception of others; this may include denial of ongoing deception, self-inflation, ego-biased social theory, false narratives of intention, and a conscious mind that operates via denial and projection to create a selfserving world. Self-deception may also result from internal representations of the voices of significant others, including parents, and may come from internal genetic conflict, the most important for our species arising from differentially imprinted maternal and paternal genes. Selection also favors suppressing negative phenotypic traits. Finally, a positive form of self-deception may serve to orient the organism favorably toward the future. Self-deception can be analyzed in groups and is done so here with special attention to its costs.

Coadaptation in mother and infant regulated by a paternally expressed imprinted gene.

by James P Curley , Sheila Barton , Azim Surani , Eric B Keverne - Proceedings of the Royal Society B: Biological Sciences , 2004
"... This study investigates how a targeted mutation of a paternally expressed imprinted gene regulates multiple aspects of foetal and post-natal development including placental size, foetal growth, suckling and post-natal growth, weaning age and puberty onset. This same mutation in a mother impairs mat ..."
Abstract - Cited by 28 (6 self) - Add to MetaCart
This study investigates how a targeted mutation of a paternally expressed imprinted gene regulates multiple aspects of foetal and post-natal development including placental size, foetal growth, suckling and post-natal growth, weaning age and puberty onset. This same mutation in a mother impairs maternal reproductive success with reduced maternal care, reduced maternal food intake during pregnancy, and impaired milk let-down, which in turn reduces infant growth and delays weaning and onset of puberty. The significance of these coadaptive traits being synchronized in mother and offspring by the same paternally expressed imprinted gene ensures that offspring that have extracted 'good' maternal nurturing will themselves be both well provisioned and genetically predisposed towards 'good' mothering.

Genomic imprinting, sex-biased dispersal, and social behavior

by David Haig - Evolutionary Perspectives on Human Reproductive Behavior , 2000
"... ABSTRACT: Some genes carry a record of the sex of the gene’s carrier in the previous generation that influences the gene’s expression in this generation. This additional information can result in intragenomic conflicts between an individual’s maternally and paternally derived alleles over behaviors ..."
Abstract - Cited by 11 (4 self) - Add to MetaCart
ABSTRACT: Some genes carry a record of the sex of the gene’s carrier in the previous generation that influences the gene’s expression in this generation. This additional information can result in intragenomic conflicts between an individual’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 sexlinked relatedness between parents and offspring of the heterogametic sex.

Evolutionary Conflicts in Pregnancy and Calcium Metabolism— A Review

by D. Haig , 2004
"... 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 hapl ..."
Abstract - Cited by 10 (0 self) - Add to MetaCart
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 ‘selfish ’ 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. � 2004 IFPA and Elsevier Ltd. All rights reserved.
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...ting predicts that paternally derived alleles are inactivated when matrilineal inclusive fitness is maximized by a higher level of gene product than that which maximizes patrilineal inclusive fitness =-=[41]-=-. Thus, the phenotypic silence of the paternal allele encoding G sα in proximal renal tubules suggests that patrilineal inclusive fitness would be increased, and matrilineal inclusive fitness decrease...

Evolution of Genomic Imprinting with Biparental Care: Implications for Prader-Willi and Angelman Syndromes PLoS

by Francisco Úbeda
"... The term ‘‘imprinted gene’ ’ refers to genes whose expression is conditioned by their parental origin. Among theories to unravel the evolution of genomic imprinting, the kinship theory prevails as the most widely accepted, because it sheds light on many aspects of the biology of imprinted genes. Whi ..."
Abstract - Cited by 7 (0 self) - Add to MetaCart
The term ‘‘imprinted gene’ ’ refers to genes whose expression is conditioned by their parental origin. Among theories to unravel the evolution of genomic imprinting, the kinship theory prevails as the most widely accepted, because it sheds light on many aspects of the biology of imprinted genes. While most assumptions underlying this theory have not escaped scrutiny, one remains overlooked: mothers are the only source of parental investment in mammals. But, is it reasonable to assume that fathers ’ contribution of resources is negligible? It is not in some key mammalian orders including humans. In this research, I generalize the kinship theory of genomic imprinting beyond maternal contribution only. In addition to deriving new conditions for the evolution of imprinting, I have found that the same gene may show the opposite pattern of expression when the investment of one parent relative to the investment of the other changes; the reversion, interestingly, does not require that fathers contribute more resources than mothers. This exciting outcome underscores the intimate connection between the kinship theory and the social structure of the organism considered. Finally, the insight gained from my model enabled me to explain the clinical phenotype of Prader-Willi syndrome. This syndrome is caused by the paternal inheritance of a deletion of the PWS/AS cluster of imprinted genes in human Chromosome 15. As such, children suffering from this syndrome exhibit a striking biphasic phenotype characterized by poor sucking and reduced weight before weaning but by voracious appetite and obesity after weaning. Interest in providing an evolutionary explanation to such phenotype is 2-fold. On the one hand, the
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...herself. After weaning, direct paternal food transfer does not leave room for the mother to manipulate paternal investment. A Model of Biparental Care In this section, I generalize the kinship theory =-=[40]-=- by allowing the expression of a gene in an offspring to affect both maternal and paternal investment (as opposed to maternal investment only). The model here presented (see the Methods section for a ...

The Maternally Expressed WRKY Transcription Factor TTG2 Controls Lethality in Interploidy Crosses of Arabidopsis

by Brian P. Dilkes, Melissa Spielman, Renate Weizbauer, Brian Watson, Rod J. Scott, Luca Comai
"... expressed WRKY transcription factor TTG2 Controls lethality in interploidy crosses of Arabidopsis. PLoS Biology, 6 (12). pp. ..."
Abstract - Cited by 6 (0 self) - Add to MetaCart
expressed WRKY transcription factor TTG2 Controls lethality in interploidy crosses of Arabidopsis. PLoS Biology, 6 (12). pp.
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...e the interploidy barrier might be under continued selection due to the ability of variation in expression to affect seed fitness [51] or purifying selection to maintain optimal expression regulation =-=[90,91]-=-. Despite these suggestions, it is possible that neutral variation, i.e., of no consequence in balanced crosses, limits fitness in the out-of-balance fertilization products produced by interploidy cro...

Evolution of the CDKN1C-KCNQ1 imprinted domain

by E I Ager, A Pask, H M Gehring, G Shaw, M Renfree - BMC Evol. Biol , 2008
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Abstract - Cited by 4 (0 self) - Add to MetaCart
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Comparative phylogenetic analysis reveals multiple non-imprinted isoforms of opossum Dlk1

by Jennifer R. Weidman, Kristin A. Maloney, Y L. Jirtle - Mamm. Genome , 2006
"... Imprinted genes are monoallelically expressed in a parent-of-origin manner and were previously identi-fied in both marsupials and eutherians, but not in monotremes. Phylogenetic comparison of imprinted domains is a powerful tool for investigating the molecular and adaptive evolution of this unique g ..."
Abstract - Cited by 3 (0 self) - Add to MetaCart
Imprinted genes are monoallelically expressed in a parent-of-origin manner and were previously identi-fied in both marsupials and eutherians, but not in monotremes. Phylogenetic comparison of imprinted domains is a powerful tool for investigating the molecular and adaptive evolution of this unique gene regulatory mechanism. Herein, we report that mul-tiple transcripts of Dlk1 (Delta, Drosophila, Homo-log-like 1) are expressed in the opossum, but none are imprinted. Thus, we provide the first example of a reciprocally imprinted gene domain in which imprinting evolved in a common ancestor to euthe-rian rather than therian mammals. Moreover, the reciprocally imprinted Meg3 (Maternally Expressed Gene 3), found downstream of Dlk1 in eutherian mammals, is absent in the opossum. We propose that the Meg3 sequence integrated into the eutherian Dlk1 domain via a LINE-1 element and that Dlk1 became imprinted in eutherian mammals only after this downstream integration. These findings clearly demonstrate that imprinted genes did not all evolve before the divergence of marsupials and eutherians.

A Maternal–Offspring Coadaptation Theory for the Evolution of Genomic Imprinting

by Jason B. Wolf, Reinmar Hager
"... Imprinted genes are expressed either from the maternally or paternally inherited copy only, and they play a key role in regulating complex biological processes, including offspring development and mother–offspring interactions. There are several competing theories attempting to explain the evolution ..."
Abstract - Cited by 3 (0 self) - Add to MetaCart
Imprinted genes are expressed either from the maternally or paternally inherited copy only, and they play a key role in regulating complex biological processes, including offspring development and mother–offspring interactions. There are several competing theories attempting to explain the evolutionary origin of this monoallelic pattern of gene expression, but a prevailing view has emerged that holds that genomic imprinting is a consequence of conflict between maternal and paternal gene copies over maternal investment. However, many imprinting patterns and the apparent overabundance of maternally expressed genes remain unexplained and may be incompatible with current theory. Here we demonstrate that sole expression of maternal gene copies is favored by natural selection because it increases the adaptive integration of offspring and maternal genomes, leading to higher offspring fitness. This novel coadaptation theory for the evolution of genomic imprinting is consistent with results of recent studies on epigenetic effects, and it provides a testable hypothesis for the origin of previously unexplained major imprinting patterns across different taxa. In conjunction with existing hypotheses, our results suggest that imprinting may have evolved due to different selective pressures at different loci. Citation: Wolf JB, Hager R (2006) A maternal–offspring coadaptation theory for the evolution of genomic imprinting. PLoS Biol 4(12): e380. DOI: 10.1371/journal.pbio.0040380

I: The influence of genomic imprinting on brain development and behavior. Evol Hum Behav 2001; 22: 385–407

by Lisa M Goos , Irwin Silverman
"... Abstract Genomic imprinting, a newly discovered and significant form of gene regulation, refers to the differential expression of a gene depending on whether it is inherited from the male or female parent. The genetic conflict theory of genomic imprinting postulates that conflicts between the genet ..."
Abstract - Cited by 2 (0 self) - Add to MetaCart
Abstract Genomic imprinting, a newly discovered and significant form of gene regulation, refers to the differential expression of a gene depending on whether it is inherited from the male or female parent. The genetic conflict theory of genomic imprinting postulates that conflicts between the genetic interests of mothers, fathers, and their offspring, as well as asymmetric genetic relationships with maternal and paternal kin, led to an evolutionary ''arms race'' within the genome, which resulted in the expression of these conflicts at the phenotypic level. This paper provides background and evidence regarding genomic imprinting and its role in brain development, describes the cognitive and behavioral phenomena that have been interpreted in terms of the genetic conflict model, and points to potential avenues of further research. D
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...he fitness costs incurred by maternal investment in each offspring are borne by the mother, as well as her genetic relatives, whose genes are now less likely to be transmitted through future reproductive events. Thus, asymmetrical degrees of relatedness between parents and offspring suggest that the action of maternal and paternal genes within an offspring may have very different consequences in terms of maternal and paternal fitness. By the same token, the actions of maternal and paternal kin may have different effects on the fitness of maternal and paternal genes in an individual offspring (Haig, 1997). Genetic conflicts such as these will tend to escalate, with each move matched by a countermove (Haig, 1993). Trivers’s original theory of parent–offspring conflict predicted that prenatal conflict between parent and child would be biochemical in nature, whereas conflict postnatally would be behavioral (Haig, 1993; Trivers, 1974). In fact, many imprinted genes have been found to regulate fetal and placental growth biochemically (Haig, 1993), much in the manner predicted by Haig and Westoby (1989). Postnatally, mother–offspring behavioral conflict can be expected at weaning, the change to a mo...

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