Evidence map›Paper›PMID 11560913›Full record

ArticleGenetics2001

Selection intensity against deleterious mutations in RNA secondary structures and rate of compensatory nucleotide substitutions.

H Innan, W Stephan

Abstract read
In one paragraph

Article in Genetics, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
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  11. Article
  12. Review
  13. Article
  14. Two types of cis-trans compensation in the evolution of transcriptional regulation.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  15. Article
  16. What role does natural selection play in speciation?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2010
    Review
  17. The rate of establishment of complex adaptations.Molecular biology and evolution · 2010
    Article
  18. The population genetics of mutations: good, bad and indifferent.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2010
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

H InnanDepartment of Biological Sciences, University of Southern California, Los Angeles, California 90089-1340, USA.
W Stephan

Funding

EVOL BY MUTATIONS WITH COMPENSATORY FITNESS INTERACTIONSR01GM058405 · NIGMS · UNIVERSITY OF ROCHESTER · PI STEPHEN, WOLFGANG · 1998 to 2000
$248k
NIGMS NIH HHS GM-58405
6 · The paper itself

Abstract

A two-locus model of reversible mutations with compensatory fitness interactions is presented; single mutations are assumed to be deleterious but neutral in appropriate combinations. The expectation of the time of compensatory nucleotide substitutions is calculated analytically for the case of tight linkage between sites. It is shown that selection increases the substitution time dramatically when selection intensity Ns > 1, where N is the diploid population size and s the selection coefficient. Computer simulations demonstrate that recombination increases the substitution time, but the effect of recombination is small when selection is weak. The amount of linkage disequilibrium generated in the process of compensatory substitution is also investigated. It is shown that significant linkage disequilibrium is expected to be rare in natural populations. The model is applied to the mRNA secondary structure of the bicoid 3' untranslated region of Drosophila. It is concluded that average selection intensity Ns against single deleterious mutations is not likely to be much larger than 1.

Indexed as

Gene DeletionMutationNucleic Acid Conformation3' Untranslated RegionsAllelesAnimalsComputer SimulationDiploidyDrosophilaDrosophila ProteinsEvolution, MolecularHomeodomain ProteinsLinkage DisequilibriumModels, GeneticModels, StatisticalRecombination, Genetic3' Untranslated Regionsbcd protein, DrosophilaDrosophila ProteinsHomeodomain ProteinsRNATrans-Activators

Identifiers

PMID11560913
PMCPMC1461802

What OpenQuestion holds

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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.