THE EVOLUTION OF EPISTASIS AND THE ADVANTAGE OF RECOMBINATION IN POPULATIONS OF BACTERIOPHAGE T4

Genetics ◽  
1977 ◽  
Vol 86 (3) ◽  
pp. 607-621
Author(s):  
Russell L Malmberg

ABSTRACT Experiments reported here test two hypotheses about the evolution of recombination: first, the Fisher-Muller concept that sexual organisms respond to selection more rapidly than do asexual ones, and second, that epistasis is more likely to evolve in the absence of recombination. Populations of bacteriophage T4 were selected by the drug proflavine in discrete generations and the change in mean population fitness was monitored. Three separate selection series yielded results supporting the Fisher-Muller hypothesis. The amount of epistasis evolved was measured by partitioning the T4 map into regions and comparing the sum of the proflavine resistances of each region with the resistance of the whole. Significantly more interactions were found in phage isolated from the populations with lower total recombination than in those from populations with higher recombination. The degree to which these experiments fit preconceived notions about natural selection suggests that microorganisms may be advantageously used in other population genetics experiments.

2021 ◽  
Author(s):  
Alexander L Cope ◽  
Premal Shah

Patterns of non-uniform usage of synonymous codons (codon bias) varies across genes in an organism and across species from all domains of life. The bias in codon usage is due to a combination of both non-adaptive (e.g. mutation biases) and adaptive (e.g. natural selection for translation efficiency/accuracy) evolutionary forces. Most population genetics models quantify the effects of mutation bias and selection on shaping codon usage patterns assuming a uniform mutation bias across the genome. However, mutation biases can vary both along and across chromosomes due to processes such as biased gene conversion, potentially obfuscating signals of translational selection. Moreover, estimates of variation in genomic mutation biases are often lacking for non-model organisms. Here, we combine an unsupervised learning method with a population genetics model of synonymous codon bias evolution to assess the impact of intragenomic variation in mutation bias on the strength and direction of natural selection on synonymous codon usage across 49 Saccharomycotina budding yeasts. We find that in the absence of a priori information, unsupervised learning approaches can be used to identify regions evolving under different mutation biases. We find that the impact of intragenomic variation in mutation bias varies widely, even among closely-related species. We show that the overall strength and direction of selection on codon usage can be underestimated by failing to account for intragenomic variation in mutation biases. Interestingly, genes falling into clusters identified by machine learning are also often physically clustered across chromosomes, consistent with processes such as biased gene conversion. Our results indicate the need for more nuanced models of sequence evolution that systematically incorporate the effects of variable mutation biases on codon frequencies.


Author(s):  
Gerard G. Dumancas

Population genetics is the study of the frequency and interaction of alleles and genes in population and how this allele frequency distribution changes over time as a result of evolutionary processes such as natural selection, genetic drift, and mutation. This field has become essential in the foundation of modern evolutionary synthesis. Traditionally regarded as a highly mathematical discipline, its modern approach comprises more than the theoretical, lab, and fieldwork. Supercomputers play a critical role in the success of this field and are discussed in this chapter.


Author(s):  
Randolph M. Nesse ◽  
Richard Dawkins

The role of evolutionary biology as a basic science for medicine is expanding rapidly. Some evolutionary methods are already widely applied in medicine, such as population genetics and methods for analysing phylogenetic trees. Newer applications come from seeking evolutionary as well as proximate explanations for disease. Traditional medical research is restricted to proximate studies of the body’s mechanism, but separate evolutionary explanations are needed for why natural selection has left many aspects of the body vulnerable to disease. There are six main possibilities: mismatch, infection, constraints, trade-offs, reproduction at the cost of health, and adaptive defences. Like other basic sciences, evolutionary biology has limited direct clinical implications, but it provides essential research methods, encourages asking new questions that foster a deeper understanding of disease, and provides a framework that organizes the facts of medicine.


Much has been learned about transposable genetic elements in Drosophila , but questions still remain, especially concerning their evolutionary significance. Three such questions are considered here, (i) Has the behaviour of transposable elements been most influenced by natural selection at the level of the organism, the population, or the elements themselves? (ii) How did the elements originate in the genome of the species? (iii) Why are laboratory stocks different from natural populations with respect to their transposable element composition? No final answers to these questions are yet available, but by focusing on the two families of hybrid dysgenesis-causing elements, the P and I factors, we can draw some tentative conclusions.


Heredity ◽  
1958 ◽  
Vol 12 (2) ◽  
pp. 145-167 ◽  
Author(s):  
Motoo Kimura

2005 ◽  
Vol 56 ◽  
pp. 105-124
Author(s):  
Michael Ruse

The homologies of process within morphogenetic fields provide some of the best evidence for evolution—just as skeletal and organ homologies did earlier. Thus, the evidence for evolution is better than ever. The role of natural selection in evolution, however, is seen to play less an important role. It is merely a filter for unsuccessful morphologies generated by development. Population genetics is destined to change if it is not to become as irrelevant to evolution as Newtonian mechanics is to contemporary physics. (Gilbert, Opitz, and Raff 1996, 368)


2019 ◽  
Vol 110 (4) ◽  
pp. 383-395 ◽  
Author(s):  
Timothée Bonnet ◽  
Michael B Morrissey ◽  
Loeske E B Kruuk

AbstractAdditive genetic variance in relative fitness (σA2(w)) is arguably the most important evolutionary parameter in a population because, by Fisher’s fundamental theorem of natural selection (FTNS; Fisher RA. 1930. The genetical theory of natural selection. 1st ed. Oxford: Clarendon Press), it represents the rate of adaptive evolution. However, to date, there are few estimates of σA2(w) in natural populations. Moreover, most of the available estimates rely on Gaussian assumptions inappropriate for fitness data, with unclear consequences. “Generalized linear animal models” (GLAMs) tend to be more appropriate for fitness data, but they estimate parameters on a transformed (“latent”) scale that is not directly interpretable for inferences on the data scale. Here we exploit the latest theoretical developments to clarify how best to estimate quantitative genetic parameters for fitness. Specifically, we use computer simulations to confirm a recently developed analog of the FTNS in the case when expected fitness follows a log-normal distribution. In this situation, the additive genetic variance in absolute fitness on the latent log-scale (σA2(l)) equals (σA2(w)) on the data scale, which is the rate of adaptation within a generation. However, due to inheritance distortion, the change in mean relative fitness between generations exceeds σA2(l) and equals (exp⁡(σA2(l))−1). We illustrate why the heritability of fitness is generally low and is not a good measure of the rate of adaptation. Finally, we explore how well the relevant parameters can be estimated by animal models, comparing Gaussian models with Poisson GLAMs. Our results illustrate 1) the correspondence between quantitative genetics and population dynamics encapsulated in the FTNS and its log-normal-analog and 2) the appropriate interpretation of GLAM parameter estimates.


In so far as it is associated with declining fertility and increasing mortality, senescence is directly detrimental to reproductive success. Natural selection should therefore act in the direction of postponing or eliminating senescence from the life history. The widespread occurrence of senescence is explained by observing that (i) the force of natural selection is generally weaker at late ages than at early ages, and (ii) the acquisition of greater longevity usually involves some cost. Two convergent theories are the ‘antagonistic pleiotropy’ theory, based in population genetics, and the ‘disposable soma’ theory, based in physiological ecology. The antagonistic pleiotropy theory proposes that certain alleles that are favoured because of beneficial early effects also have deleterious later effects. The disposable soma theory suggests that because of the competing demands of reproduction less effort is invested in the maintenance of somatic tissues than is necessary for indefinite survival.


Sign in / Sign up

Export Citation Format

Share Document