Inferring natural selection in a fossil threespine stickleback

Paleobiology ◽  
2006 ◽  
Vol 32 (4) ◽  
pp. 562-577 ◽  
Author(s):  
Michael A. Bell ◽  
Matthew P. Travis ◽  
D. Max Blouw

Inferring the causes for change in the fossil record has been a persistent problem in evolutionary biology. Three independent lines of evidence indicate that a lineage of the fossil stickleback fish Gasterosteus doryssus experienced directional natural selection for reduction of armor. Nonetheless, application to this lineage of three methods to infer natural selection in the fossil record could not exclude random process as the cause for armor change. Excluding stabilizing selection and genetic drift as the mechanisms for biostratigraphic patterns in the fossil record when directional natural selection was the actual cause is very difficult. Biostratigraphic sequences with extremely fine temporal resolution among samples and other favorable properties must be used to infer directional selection in the fossil record.

2021 ◽  
Author(s):  
Z Jafarian ◽  
S Khamse ◽  
H Afshar ◽  
Khorram Khorshid HR ◽  
A Delbari ◽  
...  

Abstract Across the human protein-coding genes, the neuron-specific gene, RASGEF1C, contains the longest (GGC)-repeat, spanning its core promoter and 5′ untranslated region (RASGEF1C-201 ENST00000361132.9). RASGEF1C expression dysregulation occurs in late-onset neurocognitive disorders (NCDs), such as Alzheimer’s disease. Here we sequenced the GGC-repeat in a sample of human subjects (N = 269), consisting of late-onset NCDs (N = 115) and controls (N = 154). We also studied the status of this STR across vertebrates. The 6-repeat allele of this repeat was the predominant allele in the controls (frequency = 0.85) and NCD patients (frequency = 0.78). The NCD genotype compartment consisted of an excess of genotypes that lacked the 6-repeat (Mid-P exact = 0.004). We also detected divergent genotypes that were present in five NCD patients and not in the controls (Mid-P exact = 0.007). This STR expanded beyond 2-repeats specifically in primates, and was at maximum length in human. We conclude that there is natural selection for the 6-repeat allele of the RASGEF1C (GGC)-repeat in human, and significant divergence from that allele in late-onset NCDs. Indication of natural selection for predominantly abundant STR alleles and divergent genotypes enhance the perspective of evolutionary biology and disease pathogenesis in human complex disorders.


Author(s):  
Tim Lewens

Students of the natural world have long remarked on the fact that animals and plants are well suited to the demands of their environments. ‘Adaptation’, as it is used in modern biology, can name both the process by which organisms acquire this functional match, and the products of that process. Eyes, wings, beaks, camouflaging skin pigmentation and so forth, are all ‘adaptations’ in this second sense. Modern biological orthodoxy follows Darwin in giving a central role to natural selection in explaining the production of adaptations such as these. This much is uncontroversial. But a number of more contentious conceptual questions are raised when we look in more detail at the relationship between natural selection and adaptation. One of these questions concerns how we should define adaptation. It is tempting to characterize adaptations as functional traits – eyes are for seeing, large beaks are for cracking tough seed-casings. This in turn has led many commentators in biology and philosophy to define adaptations as those traits which have been shaped by natural selection for their respective tasks. Others – especially biologists – have complained that such a definition trivializes Darwin’s claim that natural selection explains adaptation. This claim was meant to be an important discovery, not a definitional consequence of the meaning of ‘adaptation’. These worries naturally lead on to the issues of how natural selection itself is to be understood, how it is meant to explain adaptation, and how it should be distinguished from other important evolutionary processes. These topics have a historical dimension: is Darwin’s understanding of natural selection, and its relationship to adaptation, the same as that of today’s evolutionary biology? Textbook presentations often say yes, and this is surely legitimate if we make the comparison in broad terms. But differences emerge when we look in more detail. Darwin, for example, seems to make the ‘struggle for existence’ an essential element of natural selection. It is not clear whether this is the case in modern presentations. And Darwin’s presentation is largely neutral on the inheritance mechanism that accounts for parent/offspring resemblance, while modern presentations sometimes insist that natural selection always implies a genetic underpinning to inheritance.


1972 ◽  
Vol 19 (2) ◽  
pp. 173-176 ◽  
Author(s):  
P. D. N. Hebert ◽  
R. D. Ward ◽  
J. B. Gibson

SUMMARYThe frequencies of genetically determined electrophoretic variants of two enzyme systems in the parthenogenetic crustacean D. magna have been followed in two isolated populations. In both populations a marked excess of hetero-zygotes was found in the later samples. It is concluded that the observed changes in gene and genotypic frequencies are due to natural selection as both migration and genetic drift can be excluded.


Genetics ◽  
1975 ◽  
Vol 81 (2) ◽  
pp. 403-413
Author(s):  
John H Gillespie

ABSTRACT In the classical model of genetic drift in population genetics theory, use is made of a hypothetical "infinite-gametic pool". If, instead, the gametic pool is determined by the random number of offspring per individual, a new form of natural selection acting on the variance in offspring number occurs. A diffusion model of this selection process is derived and some of its properties are explored. It is shown that, independent of the sampling scheme used, the diffusion equation has the drift coefficient M(p) = p(1-p) (µ1-µ2 + σee2  2- σe e1  2) and the diffusion coefficient v(p) = p(1-σ) [pσee 2  2 + (1-σ)σee1  2]. It is also pointed out that the Direct Product Branching process model of genetic drift introduces a non-biological interaction between individuals and is thus inappropriate for modeling natural selection.


2022 ◽  

Cancer develops through the evolution of somatic cells in multicellular bodies. The familiar dynamics of organismal evolution, including mutations, natural selection, genetic drift, and migration, also occur among the cells of multicellular organisms. In some cases, but not all, these evolutionary processes lead to cancer. This has profound implications for both our understanding of cancer and our treatment of the disease, as well as its prevention. All of our medical interventions impose selective pressures on the heterogeneous populations of billions of cells in tumors, and tend to select for mutant cells that are resistant to the intervention, regardless of whether the intervention is a drug, radiation, the immune system, or anything else that has been tried. We will likely need evolutionary and ecological approaches to cancer to manage its evolution in response to our interventions. The field of the evolutionary biology and ecology of cancer is still young and relatively small. We are in the early stages of translating ideas and tools from evolutionary biology and ecology to study and manage cancers. There is a desperate need for more researchers with expertise in evolutionary biology and ecology to apply their skills and ideas to cancer. Currently, there are far more important questions that need to be addressed than there are people to address them.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Haoxuan Liu ◽  
Jianzhi Zhang

AbstractWhat determines the rate (μ) and molecular spectrum of mutation is a fundamental question. The prevailing hypothesis asserts that natural selection against deleterious mutations has pushed μ to the minimum achievable in the presence of genetic drift, or the drift barrier. Here we show that, contrasting this hypothesis, μ substantially exceeds the drift barrier in diverse organisms. Random mutation accumulation (MA) in yeast frequently reduces μ, and deleting the newly discovered mutator gene PSP2 nearly halves μ. These results, along with a comparison between the MA and natural yeast strains, demonstrate that μ is maintained above the drift barrier by stabilizing selection. Similar comparisons show that the mutation spectrum such as the universal AT mutational bias is not intrinsic but has been selectively preserved. These findings blur the separation of mutation from selection as distinct evolutionary forces but open the door to alleviating mutagenesis in various organisms by genome editing.


2018 ◽  
Author(s):  
Stephan Peischl ◽  
Kimberly J. Gilbert

AbstractUnderstanding the causes and consequences of range expansions or range shifts has a long history in evolutionary biology. Recent theoretical, experimental, and empirical work has identified two particularly interesting phenomena in the context of species range expansions: (i) gene surfing and the relaxation of natural selection, and (ii) spatial sorting. The former can lead to an accumulation of deleterious mutations at range edges, causing an expansion load and slowing down expansion. The latter can create gradients in dispersal-related traits along the expansion axis and cause an acceleration of expansion. We present a theoretical framework that treats spatial sorting and gene surfing as spatial versions of natural selection and genetic drift, respectively. This model allows us to study analytically how gene surfing and spatial sorting interact, and to derive the probability of fixation of pleiotropic mutations at the expansion front. We use our results to predict the co-evolution of mean fitness and dispersal rates, taking into account the effects of random genetic drift, natural selection and spatial sorting, as well as correlations between fitnessand dispersal-related traits. We identify a “rescue effect” of spatial sorting, where the evolution of higher dispersal rates at the leading edge rescues the population from incurring expansion load.


Entropy ◽  
2020 ◽  
Vol 22 (8) ◽  
pp. 907
Author(s):  
Wolfgang Stephan ◽  
Sona John

Polygenic adaptation in response to selection on quantitative traits has become an important topic in evolutionary biology. Here we review the recent literature on models of polygenic adaptation. In particular, we focus on a model that includes mutation and both directional and stabilizing selection on a highly polygenic trait in a population of finite size (thus experiencing random genetic drift). Assuming that a sudden environmental shift of the fitness optimum occurs while the population is in a stochastic equilibrium, we analyze the adaptation of the trait to the new optimum. When the shift is not too large relative to the equilibrium genetic variance and this variance is determined by loci with mostly small effects, the approach of the mean phenotype to the optimum can be approximated by a rapid exponential process (whose rate is proportional to the genetic variance). During this rapid phase the underlying changes to allele frequencies, however, may depend strongly on genetic drift. While trait-increasing alleles with intermediate equilibrium frequencies are dominated by selection and contribute positively to changes of the trait mean (i.e., are aligned with the direction of the optimum shift), alleles with low or high equilibrium frequencies show more of a random dynamics, which is expected when drift is dominating. A strong effect of drift is also predicted for population size bottlenecks. Our simulations show that the presence of a bottleneck results in a larger deviation of the population mean of the trait from the fitness optimum, which suggests that more loci experience the influence of drift.


Biologia ◽  
2017 ◽  
Vol 72 (8) ◽  
Author(s):  
Peter Vršanský ◽  
Róbert Oružinský ◽  
Danil Aristov ◽  
Dan-Dan Wei ◽  
Ľubomír Vidlička ◽  
...  

AbstractHeritably transferred genome mutations extending phenotypic variability together with natural selection (alternatively with genetic drift, draft, stability, and passive selections) are the main conditions of species evolution. Intervals with high rates of detrimental mutations are virtually absent from the fossil record due to the difficulty of identifying them. Our evidence, based on living populations indicate that insect wing deformities represent heritable hypomorphic mutations that are similar to those observed in Chernobyl and Fukushima. Newly collected assemblages from two of the major diversification intervals, the Cretaceous (J/K or K1) Yixian Formation in China and Permian/Triassic (P/T) Poldars Formation in Russia, exhibit cockroach wing deformity rates of 27% and 42.5% (


2006 ◽  
Vol 29 (4) ◽  
pp. 410-411 ◽  
Author(s):  
Bernard Crespi

Diverse evidence from genomics, epidemiology, neurophysiology, psychology, and evolutionary biology converges on simple general mechanisms, based on negative secondary effects of strong selection, for how mental disorders such as psychosis have evolved and how they are sustained.


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