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. 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.
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