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The Landscape of Mouse Meiotic Double-Strand Break Formation, Processing, and Repair

Published on Oct 1, 2016in Cell36.22
· DOI :10.1016/j.cell.2016.09.035
Julian Lange13
Estimated H-index: 13
(MSK: Memorial Sloan Kettering Cancer Center),
Shintaro Yamada4
Estimated H-index: 4
(MSK: Memorial Sloan Kettering Cancer Center)
+ 6 AuthorsScott Keeney51
Estimated H-index: 51
(Cornell University)
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Abstract
Summary Heritability and genome stability are shaped by meiotic recombination, which is initiated via hundreds of DNA double-strand breaks (DSBs). The distribution of DSBs throughout the genome is not random, but mechanisms molding this landscape remain poorly understood. Here, we exploit genome-wide maps of mouse DSBs at unprecedented nucleotide resolution to uncover previously invisible spatial features of recombination. At fine scale, we reveal a stereotyped hotspot structure—DSBs occur within narrow zones between methylated nucleosomes—and identify relationships between SPO11, chromatin, and the histone methyltransferase PRDM9. At large scale, DSB formation is suppressed on non-homologous portions of the sex chromosomes via the DSB-responsive kinase ATM, which also shapes the autosomal DSB landscape at multiple size scales. We also provide a genome-wide analysis of exonucleolytic DSB resection lengths and elucidate spatial relationships between DSBs and recombination products. Our results paint a comprehensive picture of features governing successive steps in mammalian meiotic recombination.
  • References (52)
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