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

Cell | Oct 20, 2016

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.

Pubmed ID: 27745971 RIS Download

Mesh terms: Animals | Ataxia Telangiectasia Mutated Proteins | Chromatin | DNA Breaks, Double-Stranded | DNA Methylation | DNA Repair | Endodeoxyribonucleases | Genomic Instability | Histone-Lysine N-Methyltransferase | Homologous Recombination | Meiosis | Mice | Mice, Inbred C57BL | Nucleosomes | X Chromosome | Y Chromosome

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