title: Sexual and parental antagonism shape genomic architecture.
abstract: 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.
authors.affiliation: Department of Biology, Georgetown University, , Washington DC, USA, School of Biological Sciences, Royal Holloway, University of London, , Egham, UK, Department of Organismic and Evolutionary Biology, Harvard University, , Cambridge, MA, USA.
authors.forename: Manus M
authors.initials: MM
authors.lastname: Patten
authors.forename: Francisco
authors.initials: F
authors.lastname: Ubeda
authors.forename: David
authors.initials: D
authors.lastname: Haig
mesh_terms: D000483:Alleles; D000818:Animals; D005075:Biological Evolution; D005260:Female; D056084:Genetic Fitness; D015810:Linkage Disequilibrium; D008297:Male; D052586:Mating Preference, Animal; D008957:Models, Genetic; D011110:Polymorphism, Genetic; D012641:Selection, Genetic
keywords: linkage disequilibrium; parental antagonism; sexual antagonism
references.citation: Evolution. 2010 Dec;64(12):3638-42
references.pmid: 20722728
references.citation: Theor Popul Biol. 1974 Oct;6(2):173-83
references.pmid: 4445973
references.citation: Theor Popul Biol. 1975 Jun;7(3):364-98
references.pmid: 1179266
references.citation: Nature. 2009 Dec 17;462(7275):868-74
references.pmid: 20016592
references.citation: Genetics. 2004 Aug;167(4):2083-95
references.pmid: 15342542
references.citation: Trends Ecol Evol. 2009 May;24(5):280-8
references.pmid: 19307043
references.citation: Genetics. 2012 Apr;190(4):1477-89
references.pmid: 22298707
references.citation: Genetics. 1977 Jan;85(1):171-83
references.pmid: 838269
references.citation: Genetics. 2013 Jul;194(3):663-72
references.pmid: 23733787
references.citation: Heredity (Edinb). 1971 Feb;26(1):49-63
references.pmid: 5286415
references.citation: Ann N Y Acad Sci. 2009 Jun;1168:52-71
references.pmid: 19566703
references.citation: Genetics. 1967 Oct;57(2):237-65
references.pmid: 5584566
references.citation: Genetics. 1973 Sep;75(1):213-9
references.pmid: 4762877
references.citation: PLoS Biol. 2005 Mar;3(3):e63
references.pmid: 15736976
references.citation: Evolution. 2010 May;64(5):1510-6
references.pmid: 19922443
references.citation: Philos Trans R Soc Lond B Biol Sci. 2006 Feb 28;361(1466):335-43
references.pmid: 16612891
references.citation: Genetics. 2004 Aug;167(4):1537-46
references.pmid: 15342496
references.citation: Curr Opin Cell Biol. 2007 Jun;19(3):281-9
references.pmid: 17467259
references.citation: Genetics. 2012 Feb;190(2):709-23
references.pmid: 22143919
references.citation: Genetics. 1992 Apr;130(4):899-907
references.pmid: 1582564
references.citation: Evolution. 2012 Jan;66(1):55-65
references.pmid: 22220864
references.citation: Proc Biol Sci. 2011 Mar 22;278(1707):855-62
references.pmid: 20861051
references.citation: Genetics. 1978 Dec;90(4):813-25
references.pmid: 17248876