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Michael Lynch

Researcher at Arizona State University

Publications -  457
Citations -  68107

Michael Lynch is an academic researcher from Arizona State University. The author has contributed to research in topics: Population & Mutation rate. The author has an hindex of 112, co-authored 422 publications receiving 63461 citations. Previous affiliations of Michael Lynch include University of Toronto & University of Rochester.

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Large-scale detection of in vivo transcription errors

TL;DR: A unique cDNA library preparation technique that allows error detection in natural transcripts at the transcriptome-wide level is presented and revealed a base misincorporation rate in mRNAs of ∼4 × 10−6 per site, with a very biased molecular spectrum.
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On the Formation of Novel Genes by Duplication in the Caenorhabditis elegans Genome

TL;DR: The canonical model of gene duplication postulates that novel genes arise in a two-step fashion, namely, the complete duplication of a gene followed by the gradual accumulation of mutations in one or both copies leading to an altered function.
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Genetic slippage in response to sex

TL;DR: This work describes a population of the cyclical parthenogen Daphnia pulex in which sexual reproduction induced average changes in the means of life-history characters equivalent to approximately one-tenth of a phenotypic standard deviation, and shows how random mating can induce a change in the expressed genetic variance for a quantitative trait by eliminating Hardy-Weinberg disequilibria and reducing gametic-phase disequilibrium.
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An evolutionary analysis of the helix-hairpin-helix superfamily of DNA repair glycosylases.

TL;DR: Extensive variation in the number of HhH superfamily glycosylase genes present in different genomes is observed, possibly reflecting major differences among species in the mechanisms and pathways by which damaged bases are repaired and/or disparities in the basic rates and spectra of mutation experienced by different genomes.
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Mutation, selection, and the maintenance of life-history variation in a natural population.

TL;DR: The data are consistent with the idea that the vast majority of standing genetic variance for life‐history characters may be largely a consequence of the recurrent introduction of transient cohorts of mutations that are at least conditionally deleterious and raise issues about the meaning of conventional measures of standing levels of variation for fitness‐related traits.