{"_id":"3777","publisher":"Royal Society","year":"2010","page":"1281 - 1294","scopus_import":1,"oa_version":"Submitted Version","quality_controlled":"1","date_updated":"2021-01-12T07:52:07Z","day":"27","type":"journal_article","month":"04","intvolume":"       365","date_published":"2010-04-27T00:00:00Z","doi":"10.1098/rstb.2009.0320","publist_id":"2451","date_created":"2018-12-11T12:05:07Z","status":"public","pmid":1,"publication":"Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences","external_id":{"pmid":["20308104"]},"volume":365,"acknowledgement":"I would like to thank W. G. Hill and L. Loewe for organizing this special issue, and the Royal Society and Wolfson Foundation for their support. Also, A. Kondrashov and L. Loewe gave very helpful comments that helped improve the manuscript.","issue":"1544","main_file_link":[{"url":"http://www.ncbi.nlm.nih.gov/pubmed/20308104","open_access":"1"}],"oa":1,"publication_status":"published","author":[{"first_name":"Nicholas H","id":"4880FE40-F248-11E8-B48F-1D18A9856A87","full_name":"Barton, Nicholas H","orcid":"0000-0002-8548-5240","last_name":"Barton"}],"title":"Mutation and the evolution of recombination","department":[{"_id":"NiBa"}],"language":[{"iso":"eng"}],"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","citation":{"chicago":"Barton, Nicholas H. “Mutation and the Evolution of Recombination.” <i>Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences</i>. Royal Society, 2010. <a href=\"https://doi.org/10.1098/rstb.2009.0320\">https://doi.org/10.1098/rstb.2009.0320</a>.","ieee":"N. H. Barton, “Mutation and the evolution of recombination,” <i>Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences</i>, vol. 365, no. 1544. Royal Society, pp. 1281–1294, 2010.","ista":"Barton NH. 2010. Mutation and the evolution of recombination. Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences. 365(1544), 1281–1294.","short":"N.H. Barton, Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences 365 (2010) 1281–1294.","mla":"Barton, Nicholas H. “Mutation and the Evolution of Recombination.” <i>Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences</i>, vol. 365, no. 1544, Royal Society, 2010, pp. 1281–94, doi:<a href=\"https://doi.org/10.1098/rstb.2009.0320\">10.1098/rstb.2009.0320</a>.","ama":"Barton NH. Mutation and the evolution of recombination. <i>Philosophical Transactions of the Royal Society of London Series B, Biological Sciences</i>. 2010;365(1544):1281-1294. doi:<a href=\"https://doi.org/10.1098/rstb.2009.0320\">10.1098/rstb.2009.0320</a>","apa":"Barton, N. H. (2010). Mutation and the evolution of recombination. <i>Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences</i>. Royal Society. <a href=\"https://doi.org/10.1098/rstb.2009.0320\">https://doi.org/10.1098/rstb.2009.0320</a>"},"abstract":[{"lang":"eng","text":"Under the classical view, selection depends more or less directly on mutation: standing genetic variance is maintained by a balance between selection and mutation, and adaptation is fuelled by new favourable mutations. Recombination is favoured if it breaks negative associations among selected alleles, which interfere with adaptation. Such associations may be generated by negative epistasis, or by random drift (leading to the Hill-Robertson effect). Both deterministic and stochastic explanations depend primarily on the genomic mutation rate, U. This may be large enough to explain high recombination rates in some organisms, but seems unlikely to be so in general. Random drift is a more general source of negative linkage disequilibria, and can cause selection for recombination even in large populations, through the chance loss of new favourable mutations. The rate of species-wide substitutions is much too low to drive this mechanism, but local fluctuations in selection, combined with gene flow, may suffice. These arguments are illustrated by comparing the interaction between good and bad mutations at unlinked loci under the infinitesimal model."}]}