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.Comment: Updated version, with significant revision
