scholarly journals The contribution of mutation and selection to multivariate quantitative genetic variance in an outbred population of Drosophila serrata

2021 ◽  
Vol 118 (31) ◽  
pp. e2026217118
Author(s):  
Robert J. Dugand ◽  
J. David Aguirre ◽  
Emma Hine ◽  
Mark W. Blows ◽  
Katrina McGuigan

Genetic variance is not equal for all multivariate combinations of traits. This inequality, in which some combinations of traits have abundant genetic variation while others have very little, biases the rate and direction of multivariate phenotypic evolution. However, we still understand little about what causes genetic variance to differ among trait combinations. Here, we investigate the relative roles of mutation and selection in determining the genetic variance of multivariate phenotypes. We accumulated mutations in an outbred population of Drosophila serrata and analyzed wing shape and size traits for over 35,000 flies to simultaneously estimate the additive genetic and additive mutational (co)variances. This experimental design allowed us to gain insight into the phenotypic effects of mutation as they arise and come under selection in naturally outbred populations. Multivariate phenotypes associated with more (less) genetic variance were also associated with more (less) mutational variance, suggesting that differences in mutational input contribute to differences in genetic variance. However, mutational correlations between traits were stronger than genetic correlations, and most mutational variance was associated with only one multivariate trait combination, while genetic variance was relatively more equal across multivariate traits. Therefore, selection is implicated in breaking down trait covariance and resulting in a different pattern of genetic variance among multivariate combinations of traits than that predicted by mutation and drift. Overall, while low mutational input might slow evolution of some multivariate phenotypes, stabilizing selection appears to reduce the strength of evolutionary bias introduced by pleiotropic mutation.

Genetics ◽  
2002 ◽  
Vol 162 (1) ◽  
pp. 459-471 ◽  
Author(s):  
Xu-Sheng Zhang ◽  
William G Hill

AbstractIn quantitative genetics, there are two basic “conflicting” observations: abundant polygenic variation and strong stabilizing selection that should rapidly deplete that variation. This conflict, although having attracted much theoretical attention, still stands open. Two classes of model have been proposed: real stabilizing selection directly on the metric trait under study and apparent stabilizing selection caused solely by the deleterious pleiotropic side effects of mutations on fitness. Here these models are combined and the total stabilizing selection observed is assumed to derive simultaneously through these two different mechanisms. Mutations have effects on a metric trait and on fitness, and both effects vary continuously. The genetic variance (VG) and the observed strength of total stabilizing selection (Vs,t) are analyzed with a rare-alleles model. Both kinds of selection reduce VG but their roles in depleting it are not independent: The magnitude of pleiotropic selection depends on real stabilizing selection and such dependence is subject to the shape of the distributions of mutational effects. The genetic variation maintained thus depends on the kurtosis as well as the variance of mutational effects: All else being equal, VG increases with increasing leptokurtosis of mutational effects on fitness, while for a given distribution of mutational effects on fitness, VG decreases with increasing leptokurtosis of mutational effects on the trait. The VG and Vs,t are determined primarily by real stabilizing selection while pleiotropic effects, which can be large, have only a limited impact. This finding provides some promise that a high heritability can be explained under strong total stabilizing selection for what are regarded as typical values of mutation and selection parameters.


1998 ◽  
Vol 71 (2) ◽  
pp. 161-170 ◽  
Author(s):  
ENRIQUE SANTIAGO

The infinitesimal model is extended to cover linkage in finite populations. General equations to predict the dynamics of the genetic variation under the joint effects of mutation, selection and drift are derived. Under truncation and stabilizing selection, the quadratic equations for the asymptotic genetic variance (VG) are respectivelyV2G(1+kS)+VG (Ve−2NeVm) −2NeVmVe=0andV2G(1+S)+VG (Ve+γ−2NeVm) −2NeVm(Ve+γ)=0,where Ne is the effective population size, Vm is the mutational variance, Ve is the environmental variance, γ is the parameter that measures the spread of fitness around the optimum under stabilizing selection, k is equal to i(i−x) where i is the selection intensity and x is the cut-off point under truncation selection. The term S is a function of the number of chromosomes (v) and the average chromosome length (l):formula hereThese predictions are accurate when compared with results of simulations of small populations unless the number of genes is small. The infinitesimal model reduces to the continuum of alleles model if there is no recombination between homologous chromosomes.


Genetics ◽  
2002 ◽  
Vol 161 (1) ◽  
pp. 419-433 ◽  
Author(s):  
Xu-Sheng Zhang ◽  
Jinliang Wang ◽  
William G Hill

AbstractA pleiotropic model of maintenance of quantitative genetic variation at mutation-selection balance is investigated. Mutations have effects on a metric trait and deleterious effects on fitness, for which a bivariate gamma distribution is assumed. Equations for calculating the strength of apparent stabilizing selection (Vs) and the genetic variance maintained in segregating populations (VG) were derived. A large population can hold a high genetic variance but the apparent stabilizing selection may or may not be relatively strong, depending on other properties such as the distribution of mutation effects. If the distribution of mutation effects on fitness is continuous such that there are few nearly neutral mutants, or a minimum fitness effect is assumed if most mutations are nearly neutral, VG increases to an asymptote as the population size increases. Both VG and Vs are strongly affected by the shape of the distribution of mutation effects. Compared with mutants of equal effect, allowing their effects on fitness to vary across loci can produce a much higher VG but also a high Vs (Vs in phenotypic standard deviation units, which is always larger than the ratio VP/Vm), implying weak apparent stabilizing selection. If the mutational variance Vm is ∼10-3  Ve (Ve, environmental variance), the model can explain typical values of heritability and also apparent stabilizing selection, provided the latter is quite weak as suggested by a recent review.


2020 ◽  
Author(s):  
Stéphane Chantepie ◽  
Luis-Miguel Chevin

AbstractGenetic correlations between traits can strongly impact evolutionary responses to selection, and may thus impose constraints on adaptation. Theoretical and empirical work has made it clear that, without strong linkage, genetic correlations at evolutionary equilibrium result from an interplay of correlated pleiotropic effects of mutations, and correlational selection favoring combinations of trait values. However, it is not entirely clear how the strength of stabilizing selection influences this compromise between mutation and selection effects on genetic correlations. Here, we show that the answer to this question crucially depends on the intensity of genetic drift. In large, effectively infinite populations, genetic correlations are unaffected by the strength of selection, regardless of whether the genetic architecture involves common small-effect mutations (Gaussian regime), or rare large-effect mutations (House-of-Cards regime). In contrast in finite populations, the strength of selection does affect genetic correlations, by shifting the balance from drift-dominated to selection-dominated evolutionary dynamics. The transition between these domains depends on mutation parameters to some extent, but with a similar dependence of genetic correlation on the strength of selection. Our results are particularly relevant for understanding how senescence shapes patterns of genetic correlations across ages, and genetic constraints on adaptation during colonization of novel habitats.


1988 ◽  
Vol 52 (1) ◽  
pp. 33-43 ◽  
Author(s):  
Peter D. Keightley ◽  
William G. Hill

SummaryModels of variability in quantitative traits maintained by a balance between mutation and stabilizing selection are investigated. The effects of mutant alleles are assumed to be additive and to be randomly sampled from a stationary distribution. With a two-allele model the equilibrium genetic variance in an infinite population is independent of the distribution of mutant effects, and dependent only on the total number of mutants appearing per generation. In a finite population, however, both the shape and standard deviation of the distribution of mutant effects are important. The equilibrium variance is lower when most of the mutational variance is contributed by few genes of large effect. Genes of small effect can eventually contribute substantially to the variance with increasing population size (N.) The equilibrium variance can be higher in a finite than an infinite population since near-neutral alleles can drift to intermediate frequencies where selection is weakest. Linkage leads to a reduction in the maintained variance which is small unless linkage is very tight and selection is strong, but the reduction becomes greater with increasing N since more mutants segregate. A multi-allele model is simulated and it is concluded that the two-allele model gives a good approximation of its behaviour. It is argued that the total number of loci capable of influencing most quantitative traits is large, and that the distribution of mutant effects is highly leptokurtic with the effects of most mutants very small, and such mutants are important in contributing to the maintained variance since selection against them is slight. The weakness of the simple optimum model is discussed in relation to the likely consequences of pleiotropy.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yusuke Takahashi ◽  
Anqing Zheng ◽  
Shinji Yamagata ◽  
Juko Ando

AbstractUsing a genetically informative design (about 2000 twin pairs), we investigated the phenotypic and genetic and environmental architecture of a broad construct of conscientiousness (including conscientiousness per se, effortful control, self-control, and grit). These four different measures were substantially correlated; the coefficients ranged from 0.74 (0.72–0.76) to 0.79 (0.76–0.80). Univariate genetic analyses revealed that individual differences in conscientiousness measures were moderately attributable to additive genetic factors, to an extent ranging from 62 (58–65) to 64% (61–67%); we obtained no evidence that shared environmental influences were observed. Multivariate genetic analyses showed that for the four measures used to assess conscientiousness, genetic correlations were stronger than the corresponding non-shared environmental correlations, and that a latent common factor accounted for over 84% of the genetic variance. Our findings suggest that individual differences in the four measures of conscientiousness are not distinguishable at both the phenotypic and behavioural genetic levels, and that the overlap was substantially attributable to genetic factors.


2001 ◽  
Vol 26 (1) ◽  
pp. 237-249 ◽  
Author(s):  
J.E. Pryce ◽  
R.F. Veerkamp

AbstractIn recent years there has been considerable genetic progress in milk production. Yet, increases in yield have been accompanied by an apparent lengthening of calving intervals, days open, days to first heat and a decline in conception rates, which appears to be both at the genetic and phenotypic level. Fertility has a high relative economic value compared to production traits such as protein, making it attractive to include in a breeding programme. To do this there needs to be genetic variance in fertility. Measures of fertility calculated from service dates have a small genetic compared to phenotypic variance, hence heritability estimates are small, typically less than 5%, although coefficients of genetic variance are comparable to those of production traits. Heritabilities of commencement of luteal activity determined using progesterone profiles are generally higher, and have been reported as being from 0.16 to 0.28, which could be because of a more precise quantification of genetic variance, as management influences such as delaying insemination and heat detection rates are excluded. However, it might not be the use of progesterone profiles alone, as days to first heat observed by farm staff has a heritability of 0.15. The most efficient way to breed for improved fertility is to construct a selection index using the genetic and phenotypic parameter estimates of all traits of interest in addition to their respective economic values. Index traits for fertility could include measures such as calving interval, days open, days to first service, or days to first heat but there may also be alternative measures. Examples include traits related to energy balance, such as live weight and condition score (change), both of which have higher heritabilities than fertility measures and have genetic correlations of sufficient magnitude to make genetic progress by using them feasible. To redress the balance between fertility and production, some countries already publish genetic evaluations of fertility including: Denmark, Finland, France, Germany, Israel, The Netherlands, Norway and Sweden.


1990 ◽  
Vol 55 (2) ◽  
pp. 111-117 ◽  
Author(s):  
Steven A. Frank ◽  
Montgomery Slatkin

SummaryThe Price (1970, 1972) equation is applied to the problem of describing the changes in the moments of allelic effects caused by selection, mutation and recombination at loci governing a quantitative genetic character. For comparable assumptions the resulting equations are the same as those obtained by different means by Barton & Turelli (1987; Turelli & Barton, 1989). The Price equation provides a natural framework within which to examine certain kinds of non-additive allelic effects, recombination and assortative mating. The use of the Price equation is illustrated by finding the equilibrium genetic variance under multiplicative dominance and epistasis and under assortative mating at an additive locus. The limitations of the use of recursion equations for the moments of allelic effects are also discussed.


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