Genetic recombination is targeted towards gene promoter regions in dogs

TL;DR

This study reveals that in dogs, recombination hotspots are concentrated near gene promoter regions and are independent of PRDM9, suggesting alternative mechanisms for recombination localization in mammals lacking functional PRDM9.

Contribution

The paper provides the first fine-scale recombination map for dogs, showing recombination targeting promoter regions without PRDM9 influence, contrasting with other mammals.

Findings

Recombination hotspots are near CpG-rich promoter regions in dogs.

Recombination in dogs is independent of H3K4 trimethylation marks.

Biased gene conversion may explain high CpG content in dog genome.

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.