scholarly journals Sex-Specific Selection and the Evolution of Between-Sex Genetic Covariance

2019 ◽  
Vol 110 (4) ◽  
pp. 422-432 ◽  
Author(s):  
Joel W McGlothlin ◽  
Robert M Cox ◽  
Edmund D Brodie

Abstract Because the sexes share a genome, traits expressed in males are usually genetically correlated with the same traits expressed in females. On short timescales, between-sex genetic correlations (rmf) for shared traits may constrain the evolution of sexual dimorphism by preventing males and females from responding independently to sex-specific selection. However, over longer timescales, rmf may evolve, thereby facilitating the evolution of dimorphism. Although it has been suggested that sexually antagonistic selection may reduce rmf, we lack a general theory for the evolution of rmf and its multivariate analog, the between-sex genetic covariance matrix (B). Here, we derive a simple analytical model for the within-generation change in B due to sex-specific directional selection. We present a single-trait example demonstrating that sex-specific directional selection may either increase or decrease between-sex genetic covariance, depending on the relative strength of selection in each sex and on the current value of rmf. Although sexually antagonistic selection can reduce between-sex covariance, it will only do so when selection is much stronger in one sex than in the other. Counterintuitively, sexually antagonistic selection that is equal in strength in the 2 sexes will maintain positive between-sex covariance. Selection acting in the same direction on both sexes is predicted to reduce between-sex covariance in many cases. We illustrate our model numerically using empirical measures of sex-specific selection and between-sex genetic covariance from 2 populations of sexually dimorphic brown anole lizards (Anolis sagrei) and discuss its importance for understanding the resolution of intralocus sexual conflict.

2021 ◽  
Vol 288 (1946) ◽  
pp. 20202908
Author(s):  
Leslie M. Kollar ◽  
Scott Kiel ◽  
Ashley J. James ◽  
Cody T. Carnley ◽  
Danielle N. Scola ◽  
...  

A central problem in evolutionary biology is to identify the forces that maintain genetic variation for fitness in natural populations. Sexual antagonism, in which selection favours different variants in males and females, can slow the transit of a polymorphism through a population or can actively maintain fitness variation. The amount of sexually antagonistic variation to be expected depends in part on the genetic architecture of sexual dimorphism, about which we know relatively little. Here, we used a multivariate quantitative genetic approach to examine the genetic architecture of sexual dimorphism in a scent-based fertilization syndrome of the mossCeratodon purpureus.We found sexual dimorphism in numerous traits, consistent with a history of sexually antagonistic selection. The cross-sex genetic correlations (rmf) were generally heterogeneous with many values indistinguishable from zero, which typically suggests that genetic constraints do not limit the response to sexually antagonistic selection. However, we detected no differentiation between the female- and male-specific trait (co)variance matrices (GfandGm, respectively), meaning the evolution of sexual dimorphism may be constrained. The cross-sex cross-trait covariance matrixBcontained both symmetric and asymmetric elements, indicating that the response to sexually antagonistic or sexually concordant selection, and the constraint to sexual dimorphism, are highly dependent on the traits experiencing selection. The patterns of genetic variances and covariances among these fitness components is consistent with partly sex-specific genetic architectures having evolved in order to partially resolve multivariate genetic constraints (i.e. sexual conflict), enabling the sexes to evolve towards their sex-specific multivariate trait optima.


Evolution ◽  
2006 ◽  
Vol 60 (10) ◽  
pp. 2168-2181 ◽  
Author(s):  
Matthew R. Robinson ◽  
Jill G. Pilkington ◽  
Tim H. Clutton-Brock ◽  
Josephine M. Pemberton ◽  
Loeske E.B. Kruuk

2018 ◽  
Vol 32 (12) ◽  
pp. 2678-2688 ◽  
Author(s):  
Zbyszek Boratyński ◽  
Esa Koskela ◽  
Tapio Mappes ◽  
Suzanne C. Mills ◽  
Mikael Mokkonen

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Katerina Trajanoska ◽  
Lotta J. Seppala ◽  
Carolina Medina-Gomez ◽  
Yi-Hsiang Hsu ◽  
Sirui Zhou ◽  
...  

Abstract Both extrinsic and intrinsic factors predispose older people to fall. We performed a genome-wide association analysis to investigate how much of an individual’s fall susceptibility can be attributed to genetics in 89,076 cases and 362,103 controls from the UK Biobank Study. The analysis revealed a small, but significant SNP-based heritability (2.7%) and identified three novel fall-associated loci (Pcombined ≤ 5 × 10−8). Polygenic risk scores in two independent settings showed patterns of polygenic inheritance. Risk of falling had positive genetic correlations with fractures, identifying for the first time a pathway independent of bone mineral density. There were also positive genetic correlations with insomnia, neuroticism, depressive symptoms, and different medications. Negative genetic correlations were identified with muscle strength, intelligence and subjective well-being. Brain, and in particular cerebellum tissue, showed the highest gene expression enrichment for fall-associated variants. Overall, despite the highly heterogenic nature underlying fall risk, a proportion of the susceptibility can be attributed to genetics.


2013 ◽  
Vol 93 (1) ◽  
pp. 67-77 ◽  
Author(s):  
G. Maniatis ◽  
N. Demiris ◽  
A. Kranis ◽  
G. Banos ◽  
A. Kominakis

Maniatis, G., Demiris, N., Kranis, A., Banos, G. and Kominakis, A. 2013. Model comparison and estimation of genetic parameters for body weight in commercial broilers. Can. J. Anim. Sci. 93: 67–77. The availability of powerful computing and advances in algorithmic efficiency allow for the consideration of increasingly complex models. Consequently, the development and application of appropriate statistical procedures for model evaluation is becoming increasingly important. This paper is concerned with the application of an alternative model determination criterion (conditional Akaike Information Criterion, cAIC) in a large dataset comprising 203 323 body weights of broilers, pertaining to 7 (BW7) and 35 (BW35) days of age. Seven univariate and seven bivariate models were applied. Direct genetic, maternal genetic and maternal environmental (c2) effects were estimated via REML. The model evaluation criteria included conditional Akaike Information Criterion (cAIC), Bayesian Information Criterion (BIC) and the standard Akaike Information Criterion (henceforth marginal; mAIC). According to cAIC the best-fitting model included direct genetic, maternal genetic and c2 effects. Maternal heritabilities were low (0.10 and 0.03) compared to the direct heritabilities (0.17 and 0.21), while c2 was 0.05 and 0.04 for BW7 and BW35, respectively. BIC and mAIC favoured a model that additionally included a direct-maternal genetic covariance, resulting in highly negative direct-maternal genetic correlations (−0.47 and −0.64 for BW7 and BW35, respectively) and higher direct heritabilities (0.25 and 0.28 for BW7 and BW35, respectively). Results suggest that cAIC can select different animal models than mAIC and BIC with different biological properties.


2019 ◽  
Vol 50 (14) ◽  
pp. 2385-2396 ◽  
Author(s):  
Jackson G. Thorp ◽  
Andries T. Marees ◽  
Jue-Sheng Ong ◽  
Jiyuan An ◽  
Stuart MacGregor ◽  
...  

AbstractBackgroundDepression is a clinically heterogeneous disorder. Previous large-scale genetic studies of depression have explored genetic risk factors of depression case–control status or aggregated sums of depressive symptoms, ignoring possible clinical or genetic heterogeneity.MethodsWe analyse data from 148 752 subjects of white British ancestry in the UK Biobank who completed nine items of a self-rated measure of current depressive symptoms: the Patient Health Questionnaire (PHQ-9). Genome-Wide Association analyses were conducted for nine symptoms and two composite measures. LD Score Regression was used to calculate SNP-based heritability (h2SNP) and genetic correlations (rg) across symptoms and to investigate genetic correlations with 25 external phenotypes. Genomic structural equation modelling was used to test the genetic factor structure across the nine symptoms.ResultsWe identified nine genome-wide significant genomic loci (8 novel), with no overlap in loci across symptoms. h2SNP ranged from 6% (concentration problems) to 9% (appetite changes). Genetic correlations ranged from 0.54 to 0.96 (all p < 1.39 × 10−3) with 30 of 36 correlations being significantly smaller than one. A two-factor model provided the best fit to the genetic covariance matrix, with factors representing ‘psychological’ and ‘somatic’ symptoms. The genetic correlations with external phenotypes showed large variation across the nine symptoms.ConclusionsPatterns of SNP associations and genetic correlations differ across the nine symptoms, suggesting that current depressive symptoms are genetically heterogeneous. Our study highlights the value of symptom-level analyses in understanding the genetic architecture of a psychiatric trait. Future studies should investigate whether genetic heterogeneity is recapitulated in clinical symptoms of major depression.


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