With the Correct Concept of Mutation Rate, Cluster Mutations Can Explain the Overdispersed Molecular Clock

‘What are viruses?’ introduces viruses and their structure. Martinus Beijerinck, in 1898, was the first to coin the term ‘virus’, and invention of the electron microscope in the late 1930s greatly enhanced virus identification. Viruses are not cells, but obligate parasites that must infect a cell and use its organelles in order to reproduce. They carry either DNA or RNA, and have a protein coat called a capsid. The whole structure is called a virion. Viruses have a high mutation rate, which helps them to survive and boost their resistance to antiviral drugs. The molecular clock technique to track a virus’s history is also explained.

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Human molecular evolutionary rate, time dependency and transient polymorphism effects viewed through ancient and modern mitochondrial DNA genomes

Scientific Reports ◽

10.1038/s41598-021-84583-1 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Vicente M. Cabrera

Keyword(s):

Mutation Rate ◽

Molecular Clock ◽

Substitution Rate ◽

Evolutionary Rate ◽

Evolutionary Genetics ◽

Modern Human ◽

Human Populations ◽

Time Dependency ◽

Effective Population ◽

Complete Mitochondrial Genomes

AbstractHuman evolutionary genetics gives a chronological framework to interpret the human history. It is based on the molecular clock hypothesis that suppose a straightforward relationship between the mutation rate and the substitution rate with independence of other factors as demography dynamics. Analyzing ancient and modern human complete mitochondrial genomes we show here that, along the time, the substitution rate can be significantly slower or faster than the average germline mutation rate confirming a time dependence effect mainly attributable to changes in the effective population size of the human populations, with an exponential growth in recent times. We also detect that transient polymorphisms play a slowdown role in the evolutionary rate deduced from haplogroup intraspecific trees. Finally, we propose the use of the most divergent lineages within haplogroups as a practical approach to correct these molecular clock mismatches.

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The Rate of Molecular Evolution When Mutation May Not Be Weak

10.1101/259507 ◽

2018 ◽

Cited By ~ 2

Author(s):

A.P. Jason de Koning ◽

Bianca D. De Sanctis

Keyword(s):

Natural Selection ◽

Molecular Evolution ◽

Population Size ◽

Mutation Rate ◽

Molecular Clock ◽

Neutral Theory ◽

Neutral Evolution ◽

Systematic Bias ◽

Effective Population ◽

Sequence Comparisons

AbstractOne of the most fundamental rules of molecular evolution is that the rate of neutral evolution equals the mutation rate and is independent of effective population size. This result lies at the heart of the Neutral Theory, and is the basis for numerous analytic approaches that are widely applied to infer the action of natural selection across the genome and through time, and for dating divergence events using the molecular clock. However, this result was derived under the assumption that evolution is strongly mutation-limited, and it has not been known whether it generalizes across the range of mutation pressures or the spectrum of mutation types observed in natural populations. Validated by both simulations and exact computational analyses, we present a direct and transparent theoretical analysis of the Wright-Fisher model of population genetics, which shows that some of the most important rules of molecular evolution are fundamentally changed by considering recurrent mutation’s full effect. Surprisingly, the rate of the neutral molecular clock is found to have population-size dependence and to not equal the mutation rate in general. This is because, for increasing values of the population mutation rate parameter (θ), the time spent waiting for mutations quickly becomes smaller than the cumulative time mutants spend segregating before a substitution, resulting in a net deceleration compared to classical theory that depends on the population mutation rate. Furthermore, selection exacerbates this effect such that more adaptive alleles experience a greater deceleration than less adaptive alleles, introducing systematic bias in a wide variety of methods for inferring the strength and direction of natural selection from across-species sequence comparisons. Critically, the classical weak mutation approximation performs well only when θ< 0.1, a threshold that many biological populations seem to exceed.

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Human germline mutation and the erratic evolutionary clock

10.1101/058024 ◽

2016 ◽

Cited By ~ 4

Author(s):

Priya Moorjani ◽

Ziyue Gao ◽

Molly Przeworski

Keyword(s):

Human Evolution ◽

Mutation Rate ◽

Germline Mutation ◽

Molecular Clock ◽

Mutation Rates ◽

Evolutionary Lineage ◽

Precise Characterization ◽

Evolutionary Clock ◽

Males And Females

AbstractOur understanding of the chronology of human evolution relies on the “molecular clock” provided by the steady accumulation of substitutions on an evolutionary lineage. Recent analyses of human pedigrees have called this understanding into question, by revealing unexpectedly low germline mutation rates, which imply that substitutions accrue more slowly than previously believed. Translating mutation rates estimated from pedigrees into substitution rates is not as straightforward as it may seem, however. We dissect the steps involved, emphasizing that dating evolutionary events requires not “a mutation rate,” but a precise characterization of how mutations accumulate in development, in males and females—knowledge that remains elusive.

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Human Molecular Evolutive Rate, Time Dependency and Transient Polymorphism Effects Viewed Through Ancient and Modern Mitochondrial DNA Genomes.

10.21203/rs.3.rs-110235/v1 ◽

2020 ◽

Author(s):

Vicente Cabrera

Keyword(s):

Mutation Rate ◽

Molecular Clock ◽

Evolutionary Genetics ◽

Modern Human ◽

Mitochondrial Genomes ◽

Human Populations ◽

Time Dependency ◽

Effective Population ◽

Molecular Clock Hypothesis ◽

Complete Mitochondrial Genomes

Abstract Human evolutionary genetics gives a chronological framework to interpret the human history. It is based on the molecular clock hypothesis that suppose a straightforward relationship between the pace of the mutation rate and the evolutive rate with independence of other factors as demography dynamics. Analyzing ancient and modern human complete mitochondrial genomes we constate here that, along the time, the evolutive rate can be significantly slower or faster than the average germline mutation rate confirming a time dependence effect mainly attributable to changes in the effective population size of the human populations, with an exponential growth in recent times. We also detect that transient polymorphisms play a slowdown role in the evolutive rate deduced from haplogroup intraspecific trees. Finally, we propose the use of the most evolved lineages within haplogroups as a practical approach to correct these molecular clock mismatches.

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