期刊
NATURE STRUCTURAL & MOLECULAR BIOLOGY
卷 18, 期 1, 页码 56-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nsmb.1946
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资金
- US National Institutes of Health [CA100839, MH084119]
- Leukemia and Lymphoma Society Scholar Award [1054-09]
- US National Institute of Diabetes and Digestive and Kidney Diseases
- NATIONAL CANCER INSTITUTE [R56CA100839, R01CA100839] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [ZIADK052032] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [R03MH084119] Funding Source: NIH RePORTER
The ubiquitously expressed Rad51 recombinase and the meiosis-specific Dmc1 recombinase promote the formation of strand-invasion products (D-loops) between homologous molecules. Strand-invasion products are processed by either the double-strand break repair (DSBR) or synthesis-dependent strand annealing (SDSA) pathway. D-loops destined to be processed by SDSA need to dissociate, producing non-crossovers, and those destined for DSBR should resist dissociation to generate crossovers. The mechanism that channels recombination intermediates into different homologous-recombination pathways is unknown. Here we show that D-loops in a human DMC1-driven reaction are substantially more resistant to dissociation by branch-migration proteins such as RAD54 than those formed by RAD51. We propose that the intrinsic resistance to dissociation of DMC1 strand-invasion intermediates may account for why DMC1 is essential to ensure the proper segregation of chromosomes in meiosis.
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