Journal
NATURE COMMUNICATIONS
Volume 11, Issue 1, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41467-020-16885-3
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Funding
- Deutsche Forschungsgemeinschaft (DFG) [TO421/3-1/2, TO421/5-1, TO421/6-1/2, TO421/7-1, TO421/8-1/2, TO421/10-1, TO421/11-1, TO421/12-1]
- HFSP research grant [RGP0008/2015]
- DIGS-BB wrap up programme
- ERASMUS
- Boehringer Ingelheim GmbH
- Austrian Academy of Sciences
- Japan Society for the Promotion of Science
- National Key Research and Development Program of China [2019YFE0106700]
- Howard Hughes Medical Institute
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Orderly chromosome segregation is enabled by crossovers between homologous chromosomes in the first meiotic division. Crossovers arise from recombination-mediated repair of programmed DNA double-strand breaks (DSBs). Multiple DSBs initiate recombination, and most are repaired without crossover formation, although one or more generate crossovers on each chromosome. Although the underlying mechanisms are ill-defined, the differentiation and maturation of crossover-specific recombination intermediates requires the cyclin-like CNTD1. Here, we identify PRR19 as a partner of CNTD1. We find that, like CNTD1, PRR19 is required for timely DSB repair and the formation of crossover-specific recombination complexes. PRR19 and CNTD1 co-localise at crossover sites, physically interact, and are interdependent for accumulation, indicating a PRR19-CNTD1 partnership in crossing over. Further, we show that CNTD1 interacts with a cyclin-dependent kinase, CDK2, which also accumulates in crossover-specific recombination complexes. Thus, the PRR19-CNTD1 complex may enable crossover differentiation by regulating CDK2. Crossing over is a critical process during meiosis, although the regulation of this process still remains somewhat elusive. Here, the authors show that PRR19 partners with CNTD1 to enable formation of crossover-specific recombination complexes in mouse germ cells.
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