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      A genomic region containingRNF212andCPLX1is associated with sexually-dimorphic recombination rate variation in wild Soay sheep (Ovis aries).

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          Abstract

          Meiotic recombination breaks down linkage disequilibrium and forms new haplotypes, meaning that it is an important driver of diversity in eukaryotic genomes. Understanding the causes of variation in recombination rate is important in interpreting and predicting evolutionary phenomena and for understanding the potential of a population to respond to selection. However, despite attention in model systems, there remains little data on how recombination rate varies at the individual level in natural populations. Here, we used extensive pedigree and high-density SNP information in a wild population of Soay sheep ( Ovis aries) to investigate the genetic architecture of individual autosomal recombination rate. Individual rates were high relative to other mammal systems, and were higher in males than in females (autosomal map lengths of 3748 cM and 2860 cM, respectively). The heritability of autosomal recombination rate was low but significant in both sexes (h 2= 0.16 & 0.12 in females and males, respectively). In females, 46.7% of the heritable variation was explained by a sub-telomeric region on chromosome 6; a genome-wide association study showed the strongest associations at the locus RNF212, with further associations observed at a nearby ~374kb region of complete linkage disequilibrium containing three additional candidate loci, CPLX1, GAKand PCGF3. A second region on chromosome 7 containing REC8and RNF212Bexplained 26.2% of the heritable variation in recombination rate in both sexes. Comparative analyses with 40 other sheep breeds showed that haplotypes associated with recombination rates are both old and globally distributed. Both regions have been implicated in rate variation in mice, cattle and humans, suggesting a common genetic architecture of recombination rate variation in mammals.

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          Author and article information

          Journal
          bioRxiv
          August 17 2015
          Article
          10.1101/024869
          a646bb93-0303-4e5d-bf87-6e9a05bdb513
          © 2015
          History

          Human biology,Genetics
          Human biology, Genetics

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