Evidence map›Paper›PMID 12590655›Full record

ArticleBMC evolutionary biology2003

Compensatory mutations cause excess of antagonistic epistasis in RNA secondary structure folding.

Claus O Wilke, Richard E Lenski, Christoph Adami

Abstract read
In one paragraph

Article in BMC evolutionary biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 2 pooled it
–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, 2 syntheses or guidelines pooled it.

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  13. Intramolecular phenotypic capacitance in a modular RNA molecule.Proceedings of the National Academy of Sciences of the United States of America · 2015
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  18. Interactions between evolutionary processes at high mutation rates.Evolution; international journal of organic evolution · 2012
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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

3 authors.

Claus O WilkeDigital Life Laboratory 136-93, California Institute of Technology, Pasadena, CA 91125, USA. wilke@caltech.edu
Richard E Lenski
Christoph Adami

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe rate at which fitness declines as an organism's genome accumulates random mutations is an important variable in several evolutionary theories. At an intuitive level, it might seem natural that random mutations should tend to interact synergistically, such that the rate of mean fitness decline accelerates as the number of random mutations is increased. However, in a number of recent studies, a prevalence of antagonistic epistasis (the tendency of multiple mutations to have a mitigating rather than reinforcing effect) has been observed.

resultsWe studied in silico the net amount and form of epistatic interactions in RNA secondary structure folding by measuring the fraction of neutral mutants as a function of mutational distance d. We found a clear prevalence of antagonistic epistasis in RNA secondary structure folding. By relating the fraction of neutral mutants at distance d to the average neutrality at distance d, we showed that this prevalence derives from the existence of many compensatory mutations at larger mutational distances.

conclusionsOur findings imply that the average direction of epistasis in simple fitness landscapes is directly related to the density with which fitness peaks are distributed in these landscapes.

Indexed as

Epistasis, GeneticMutationNucleic Acid ConformationAnimalsComputer SimulationDNA Mutational AnalysisEvolution, MolecularGenetic VariationGenomeGenotypeHumansModels, GeneticModels, TheoreticalMutagenesisRNASoftwareRNA

Identifiers

PMID12590655
PMCPMC149451

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.