Do you want to publish a course? Click here

Sex-specific recombination rates and allele frequencies affect the invasion of sexually antagonistic variation on autosomes

87   0   0.0 ( 0 )
 Added by Minyoung Wyman
 Publication date 2013
  fields Biology
and research's language is English




Ask ChatGPT about the research

The introduction and persistence of novel sexually antagonistic alleles can depend upon factors that differ between males and females. Understanding the conditions for invasion in a two-locus model can elucidate these processes. For instance, selection can act differently upon the sexes, or sex-linkage can facilitate the invasion of genetic variation with opposing fitness effects between the sexes. Two factors that deserve further attention are recombination rates and allele frequencies -- both of which can vary substantially between the sexes. We find that sex-specific recombination rates in a two-locus diploid model can affect the invasion outcome of sexually antagonistic alleles and that the sex-averaged recombination rate is not necessarily sufficient to predict invasion. We confirm that the range of permissible recombination rates is smaller in the sex benefitting from invasion and larger in the sex harmed by invasion. However, within the invasion space, male recombination rate can be greater than, equal to, or less than female recombination rate in order for a male-benefit, female-detriment allele to invade (and similarly for a female-benefit, male-detriment allele). We further show that a novel, sexually antagonistic allele that is also associated with a lowered recombination rate can invade more easily when present in the double heterozygote genotype. Finally, we find that sexual dimorphism in resident allele frequencies can impact the invasion of new sexually antagonistic alleles at a second locus. Our results suggest that accounting for sex-specific recombination rates and allele frequencies can determine the difference between invasion and non-invasion of novel sexually antagonistic alleles in a two-locus model.



rate research

Read More

The stationary distribution of the diffusion limit of the 2-island, 2-allele Wright-Fisher with small but otherwise arbitrary mutation and migration rates is investigated. Following a method developed by Burden and Tang (2016, 2017) for approximating the forward Kolmogorov equation, the stationary distribution is obtained to leading order as a set of line densities on the edges of the sample space, corresponding to states for which one island is bi-allelic and the other island is non-segregating, and a set of point masses at the corners of the sample space, corresponding to states for which both islands are simultaneously non-segregating. Analytic results for the corner probabilities and line densities are verified independently using the backward generator and for the corner probabilities using the coalescent.
A forward diffusion equation describing the evolution of the allele frequency spectrum is presented. The influx of mutations is accounted for by imposing a suitable boundary condition. For a Wright-Fisher diffusion with or without selection and varying population size, the boundary condition is $lim_{x downarrow 0} x f(x,t)=theta rho(t)$, where $f(cdot,t)$ is the frequency spectrum of derived alleles at independent loci at time $t$ and $rho(t)$ is the relative population size at time $t$. When population size and selection intensity are independent of time, the forward equation is equivalent to the backwards diffusion usually used to derive the frequency spectrum, but the forward equation allows computation of the time dependence of the spectrum both before an equilibrium is attained and when population size and selection intensity vary with time. From the diffusion equation, we derive a set of ordinary differential equations for the moments of $f(cdot,t)$ and express the expected spectrum of a finite sample in terms of those moments. We illustrate the use of the forward equation by considering neutral and selected alleles in a highly simplified model of human history. For example, we show that approximately 30% of the expected heterozygosity of neutral loci is attributable to mutations that arose since the onset of population growth in roughly the last $150,000$ years.
390 - Dirson Jian Li 2018
Based on statistical analysis of the complete genome sequences, a remote relationship has been observed between the evolution of the genetic code and the three domain tree of life. The existence of such a remote relationship need to be explained. The unity of the living system throughout the history of life relies on the common features of life: the homochirality, the genetic code and the universal genome format. The universal genome format has been observed in the genomic codon distributions as a common feature of life at the sequence level. A main aim of this article is to reconstruct and to explain the Phanerozoic biodiversity curve. It has been observed that the exponential growth rate of the Phanerozoic biodiversity curve is about equal to the exponential growth rate of genome size evolution. Hence it is strongly indicated that the expansion of genomes causes the exponential trend of the Phanerozoic biodiversity curve, where the conservative property during the evolution of life is guaranteed by the universal genome format at the sequence level. In addition, a consensus curve based on the climatic and eustatic data is obtained to explain the fluctuations of the Phanerozoic biodiversity curve. Thus, the reconstructed biodiversity curve based on genomic, climatic and eustatic data agrees with Sepkoskis curve based on fossil data. The five mass extinctions can be discerned in this reconstructed biodiversity curve, which indicates a tectonic cause of the mass extinctions. And the declining origination rate and extinction rate throughout the Phanerozoic eon might be due to the growth trend in genome size evolution.
The two classic theories for the existence of sexual replication are that sex purges deleterious mutations from a population, and that sex allows a population to adapt more rapidly to changing environments. These two theories have often been presented as opposing explanations for the existence of sex. Here, we develop and analyze evolutionary models based on the asexual and sexual replication pathways in Saccharomyces cerevisiae (Bakers yeast), and show that sexual replication can both purge deleterious mutations in a static environment, as well as lead to faster adaptation in a dynamic environment. This implies that sex can serve a dual role, which is in sharp contrast to previous theories.
The advent of accessible ancient DNA technology now allows the direct ascertainment of allele frequencies in ancestral populations, thereby enabling the use of allele frequency time series to detect and estimate natural selection. Such direct observations of allele frequency dynamics are expected to be more powerful than inferences made using patterns of linked neutral variation obtained from modern individuals. We develop a Bayesian method to make use of allele frequency time series data and infer the parameters of general diploid selection, along with allele age, in non-equilibrium populations. We introduce a novel path augmentation approach, in which we use Markov chain Monte Carlo to integrate over the space of allele frequency trajectories consistent with the observed data. Using simulations, we show that this approach has good power to estimate selection coefficients and allele age. Moreover, when applying our approach to data on horse coat color, we find that ignoring a relevant demographic history can significantly bias the results of inference. Our approach is made available in a C++ software package.
comments
Fetching comments Fetching comments
mircosoft-partner

هل ترغب بارسال اشعارات عن اخر التحديثات في شمرا-اكاديميا