A high-resolution map of non-crossover events reveals impacts of genetic diversity on mammalian meiotic recombination

Ran Li, Emmanuelle Bitoun, Nicolas Altemose, Robert W. Davies, Benjamin Davies and Simon R. Myers ()
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Ran Li: Roosevelt Drive, University of Oxford
Emmanuelle Bitoun: Roosevelt Drive, University of Oxford
Nicolas Altemose: Roosevelt Drive, University of Oxford
Robert W. Davies: Roosevelt Drive, University of Oxford
Benjamin Davies: Roosevelt Drive, University of Oxford
Simon R. Myers: Roosevelt Drive, University of Oxford

Nature Communications, 2019, vol. 10, issue 1, 1-15

Abstract: Abstract During meiotic recombination, homologue-templated repair of programmed DNA double-strand breaks (DSBs) produces relatively few crossovers and many difficult-to-detect non-crossovers. By intercrossing two diverged mouse subspecies over five generations and deep-sequencing 119 offspring, we detect thousands of crossover and non-crossover events genome-wide with unprecedented power and spatial resolution. We find that both crossovers and non-crossovers are strongly depleted at DSB hotspots where the DSB-positioning protein PRDM9 fails to bind to the unbroken homologous chromosome, revealing that PRDM9 also functions to promote homologue-templated repair. Our results show that complex non-crossovers are much rarer in mice than humans, consistent with complex events arising from accumulated non-programmed DNA damage. Unexpectedly, we also find that GC-biased gene conversion is restricted to non-crossover tracts containing only one mismatch. These results demonstrate that local genetic diversity profoundly alters meiotic repair pathway decisions via at least two distinct mechanisms, impacting genome evolution and Prdm9-related hybrid infertility.

Date: 2019
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DOI: 10.1038/s41467-019-11675-y

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