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Drive Against Hotspot Motifs in Primates Implicates the PRDM9 Gene in Meiotic Recombination

Source: Science 327, 876 (2010); doi:10.1126/science.1182363

Published December 31, 2009

PUBLICATION DATA
ISSN:
1553-9628 (online)
Publisher:
AIP is a member of CrossRef AAAS
Simon Myers,ff1,ff2 Rory Bowden,ff1,ff2 Afidalina Tumian,ff1 Ronald E. Bontrop,ff3 Colin Freeman,ff2 Tammie S. MacFie,ff4 Gil McVean,ff1,ff2 and Peter Donnellyff1,ff2
ff1Department of Statistics, Oxford University, 1 South Parks Road, Oxford OX1 3TG, UK.
ff2Wellcome Trust Centre for Human Genetics, Oxford University, Roosevelt Drive, Oxford OX3 7BN, UK.
ff3Department of Comparative Genetics and Refinement, Biomedical Primate Research Center, Lange Kleiweg 139 2288 GJ, Rijswijk, Netherlands.
ff4Department of Zoology, University of Cambridge, Downing Street, Cambridge CB2 3EJ, UK.

Although present in both humans and chimpanzees, recombination hotspots, at which meiotic crossover events cluster, differ markedly in their genomic location between the species. We report that a 13–base pair sequence motif previously associated with the activity of 40% of human hotspots does not function in chimpanzees and is being removed by self-destructive drive in the human lineage. Multiple lines of evidence suggest that the rapidly evolving zinc-finger protein PRDM9 binds to this motif and that sequence changes in the protein may be responsible for hotspot differences between species. The involvement of PRDM9, which causes histone H3 lysine 4 trimethylation, implies that there is a common mechanism for recombination hotspots in eukaryotes but raises questions about what forces have driven such rapid change. ©2010 American Association for the Advancement of Science

(As supplied by publisher.)

History: Received September 23, 2009; accepted December 17, 2009; published December 31, 2009
Permalink: http://dx.doi.org/10.1126/science.1182363
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