Genetic recombination is targeted towards gene promoter regions in dogs
Adam Auton, Ying Rui Li, Jeffrey Kidd, Kyle Oliveira, Julie Nadel, J. Kim Holloway, Jessica J. Howard, Paula E. Cohen, John M. Greally, Jun Wang, Carlos D. Bustamante, Adam R. Boyko
(Submitted on 28 May 2013)
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. Compared to genetic maps obtained in other mammalian species, the canine map is notably different at the fine-scale. While broad-scale patterns exhibit typical properties, our fine-scale estimates indicate that recombination is more uniformly distributed than has been observed in other mammalian species. In addition, 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. Finally, 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.