In the Light of Evolution Volume V: Cooperation and Conflict (2011) / Chapter Skim
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13 Pathology from Evolutionary Conflict, with a Theory of X Chromosome Versus Autosome Conflict over Sexually Antagonistic Traits--STEVEN A. FRANK and BERNARD J. CRESPI
13 Pathology from Evolutionary Conflict, with a Theory of X Chromosome Versus Autosome Conflict over Sexually Antagonistic Traits--STEVEN A. FRANK and BERNARD J. CRESPI
Pages 275-298
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From page 275... ...
For many traits, the different sexes favor different phenotypic values, and constraints prevent completely distinct expression in the sexes. In this case of sexual antagonism, we present a theory of conflict between X-linked genes and autosomal genes.
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From page 276... ...
We discuss several examples of evo lutionary conflicts, the ways in which conflict may lead to exaggerated opposition of forces on a trait, and the occasional breakdown in the normal balance of opposing forces that leads to pathology. We also present a theory of evolutionary conflict between X-linked and autosomal genes over traits that differ in their consequences for male and female fitness.
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From page 277... ...
The fifth section presents our theory of X versus autosome conflict. For a trait expressed in both sexes, the autosomes typically favor an intermediate expression that weights equally the best trait expression in males and females.
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From page 278... ...
Between conflicting parties, the greater the divergence of favored trait values is, the greater the tendency for a trait to be the outcome of a precarious balance between strongly opposed forces.
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From page 279... ...
This exaggeration of forces may be difficult to see, because the observed character value may be nearly unchanged under the stronger opposing forces that continue to balance at essentially the same level.
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From page 280... ...
In mice, this gene is perhaps the most important stimulator of fetal growth and determinant of offspring size. The paternally imprinted and maternally expressed gene H19 produces a noncoding RNA associated with reduced expression of IGF2 and a lower rate of growth (Gabory et al., 2009)
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From page 281... ...
An indirect link between imprinting and childhood cancer comes from the association between higher birth weight, accelerated fetal growth, and higher rates of most of the major childhood cancers (Troisi et al., 2006; Milne et al., 2007; Laurvick et al., 2008; Callan and Milne, 2009; Samuelsen et al., 2009)
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From page 282... ...
In their analysis of mouse brains, they estimated that >1,300 loci have the kind of parent-of-origin effects typical of imprinting. If widespread imprinting does in fact occur, then the conflicting interests of mothers and fathers over offspring growth may indeed lead to a growth regulation system precariously poised between strongly opposing forces.
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From page 283... ...
, whereas PWS individuals usually lose function of normally paternally expressed factors in the same chromosomal region (Haig and Wharton, 2003)
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From page 284... ...
The balance arises mechanistically from the relative dominance between the "selfish" limbic and the "social" neo cortical brain systems. Paternally expressed genes tend to push for greater growth and enhanced demand on maternal resources associated with enhancement of placentation, growth factors, suckling, tongue, orofacial muscles, and engagement with mother in infancy.
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From page 285... ...
CONFLICT BETWEEN THE SEXES The previous sections discussed conflict over offspring growth rate. In that case, the conflict occurs between maternally and paternally derived genes over the expression of traits within the offspring.
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From page 286... ...
Crespi which X-linked and autosomal genes are favored to push in opposite d irections on traits with different effects on male and female fitness. Sexual Conflict: Sex-Limited Traits Many traits arise from male–female interaction.
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From page 287... ...
All genes on the autosomes favor an equal weighting of the male and female optima, because the reproductive value of those autosomal genes is the same in both sexes. By contrast, genes on the X chromosome favor weighting the female optimum twice as strongly as the male optimum, because X-linked genes in females have twice the reproductive value of X-linked genes in males.
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From page 288... ...
brief comments, we could not find in the literature mention of the conflict between different genomic subsets, such as the X and the autosomes, over divergent male–female optima. Given the very simple logic of the conflict, it is not clear why the extensive discussions of sexual antagonism have not emphasized this particular aspect of X versus autosome conflict.
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From page 289... ...
The most obvious prediction is widespread interaction between X–linked and autosomal genes over sexually antagonistic traits, with the X–linked genes pushing toward the female optimum and the autosomal genes pushing toward the male optimum. However, it may be difficult to see those sorts o f interactions in a particular population.
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From page 290... ...
Increasing evidence supports this conflict interpretation for the regu lation of early offspring growth in mammals. The interesting question is: How often is the evolutionary design of regulatory control dominated by the precarious balance of conflicting and exaggerated forces rather than by the efficiency and robustness of control?
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From page 291... ...
Thus, the X versus autosome conflict may be particularly associated with widely dispersed genetic interactions throughout the genome, providing another hypothesis for rapid evolution and hybrid incompatibilities between species involving the X chromosome. In all cases of disrupted conflict, the particular disease pathologies are interesting in themselves.
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From page 292... ...
The first party has optimal trait value, mA, and the second party has optimal trait value, mB. The expected fitness of each party is given by wi = K − a ( xA + xB − mi )
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From page 293... ...
The reproductive value of X-linked genes is twice as great in females as in males, compared with the equal reproductive value weighting of the two sexes by autosomal genes. Thus, X-linked genes pull toward the female optimum and, relative to the X, autosomal genes pull in the other direction toward the male o ptimum.
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From page 294... ...
2, with α as the weighting of the fitness penalty for dis tance from the optimum trait value. The last term is a penalty for divergent contributions of the X and autosomal genes, as in Appendix A
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From page 295... ...
That correla tion causes an unexpressed (inactivated or imprinted) X-linked copy to have its fitness associated with its own latent trait value, adding a further push toward the female optimum and creating once again a conflict between X-linked and autosomal genes, including X-linked loci subject to X inactivation.
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From page 296... ...
However, the particular problem of X versus autosome conflict remains to be studied in full genetical detail.
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From page 297... ...
Pathology from Evolutionary Conflict / 297 ACKNOWLEDGMENTS S.A.F.'s research is supported by National Science Foundation Grant EF-0822399, National Institute of General Medical Sciences Models of Infectious Disease Agent Study Program Grant U01-GM-76499, and a grant from the James S McDonnell Foundation.
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