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PLoS Genet. 2013;9(12):e1003984. doi: 10.1371/journal.pgen.1003984. Epub 2013 Dec 12.

Genetic recombination is targeted towards gene promoter regions in dogs.

Author information

1
Department of Genetics, Albert Einstein College of Medicine, Bronx, New York, New York, United States of America.
2
BGI-Shenzhen, Shenzhen, China.
3
Department of Human Genetics, University of Michigan, Ann Arbor, Michigan, United States of America.
4
Department of Biomedical Sciences, Cornell University College of Veterinary Medicine, Ithaca, New York, United States of America.
5
Department of Genetics, Stanford University, Stanford, California, United States of America.

Abstract

The identification of the H3K4 trimethylase, PRDM9, as the gene responsible for recombination hotspot localization has provided considerable insight into the mechanisms by which recombination is initiated in mammals. However, uniquely amongst mammals, canids appear to lack a functional version of PRDM9 and may therefore provide a model for understanding recombination that occurs in the absence of PRDM9, and thus how PRDM9 functions to shape the recombination landscape. We have constructed a fine-scale genetic map from patterns of linkage disequilibrium assessed using high-throughput sequence data from 51 free-ranging dogs, Canis lupus familiaris. While broad-scale properties of recombination appear similar to other mammalian species, our fine-scale estimates indicate that canine highly elevated recombination rates are observed in the vicinity of CpG rich regions including gene promoter regions, but show little association with H3K4 trimethylation marks identified in spermatocytes. By comparison to genomic data from the Andean fox, Lycalopex culpaeus, we show that biased gene conversion is a plausible mechanism by which the high CpG content of the dog genome could have occurred.

PMID:
24348265
PMCID:
PMC3861134
DOI:
10.1371/journal.pgen.1003984
[Indexed for MEDLINE]
Free PMC Article

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