Evidence map›Paper›PMID 22209901›Full record

ArticleGenetics2012

Estimating the distribution of selection coefficients from phylogenetic data using sitewise mutation-selection models.

Asif U Tamuri, Mario dos Reis, Richard A Goldstein

Abstract read
In one paragraph

Article in Genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

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63citing papers in PubMed
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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

Who cites it

63 citing papers in PubMed.

  1. Article
  2. Separating selection from mutation in antibody language models.bioRxiv : the preprint server for biology · 2025
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3 more citing papers are in PubMed but not listed here.

4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Asif U TamuriMedical Research Council National Institute for Medical Research, London, NW7 1AA, United Kingdom.
Mario dos Reis
Richard A Goldstein

Funding

Biotechnology and Biological Sciences Research CouncilMedical Research Council MC_U117573805Wellcome Trust
6 · The paper itself

Abstract

Estimation of the distribution of selection coefficients of mutations is a long-standing issue in molecular evolution. In addition to population-based methods, the distribution can be estimated from DNA sequence data by phylogenetic-based models. Previous models have generally found unimodal distributions where the probability mass is concentrated between mildly deleterious and nearly neutral mutations. Here we use a sitewise mutation-selection phylogenetic model to estimate the distribution of selection coefficients among novel and fixed mutations (substitutions) in a data set of 244 mammalian mitochondrial genomes and a set of 401 PB2 proteins from influenza. We find a bimodal distribution of selection coefficients for novel mutations in both the mitochondrial data set and for the influenza protein evolving in its natural reservoir, birds. Most of the mutations are strongly deleterious with the rest of the probability mass concentrated around mildly deleterious to neutral mutations. The distribution of the coefficients among substitutions is unimodal and symmetrical around nearly neutral substitutions for both data sets at adaptive equilibrium. About 0.5% of the nonsynonymous mutations and 14% of the nonsynonymous substitutions in the mitochondrial proteins are advantageous, with 0.5% and 24% observed for the influenza protein. Following a host shift of influenza from birds to humans, however, we find among novel mutations in PB2 a trimodal distribution with a small mode of advantageous mutations.

Indexed as

Models, GeneticMutationPhylogenySelection, GeneticAlgorithmsAnimalsComputer SimulationEvolution, MolecularGenetic DriftHumansReproducibility of Results

Identifiers

PMID22209901
PMCPMC3296245

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.