Journal
EMBO JOURNAL
Volume 36, Issue 17, Pages 2488-2509Publisher
WILEY
DOI: 10.15252/embj.201695895
Keywords
Dbf4-dependent Cdc7 kinase; homologous recombination; meiosis; Polo-like kinase; synaptonemal complex
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Funding
- Biotechnology and Biological Sciences Research Council [BB/I009159/1]
- Japan Society for the Promotion of Science (JSPS) [16H07422]
- Medical Research Council doctoral studentship
- JSPS [15H059749, 16H06160]
- NIH [GM111715]
- Biotechnology and Biological Sciences Research Council [BB/I009159/1] Funding Source: researchfish
- BBSRC [BB/I009159/1] Funding Source: UKRI
- Grants-in-Aid for Scientific Research [15K21761, 16H01404, 16H06160, 16H07422] Funding Source: KAKEN
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The synaptonemal complex (SC) is a proteinaceous macromolecular assembly that forms during meiotic prophase I and mediates adhesion of paired homologous chromosomes along their entire lengths. Although prompt disassembly of the SC during exit from prophase I is a landmark event of meiosis, the underlying mechanism regulating SC destruction has remained elusive. Here, we show that DDK (Dbf4-dependent Cdc7 kinase) is central to SC destruction. Upon exit from prophase I, Dbf4, the regulatory subunit of DDK, directly associates with and is phosphorylated by the Polo-like kinase Cdc5. In parallel, upregulated CDK1 activity also targets Dbf4. An enhanced Dbf4-Cdc5 interaction pronounced phosphorylation of Dbf4 and accelerated SC destruction, while reduced/ abolished Dbf4 phosphorylation hampered destruction of SC proteins. SC destruction relieved meiotic inhibition of the ubiquitous recombinase Rad51, suggesting that the mitotic recombination machinery is reactivated following prophase I exit to repair any persisting meiotic DNA double-strand breaks. Taken together, we propose that the concerted action of DDK, Polo-like kinase, and CDK1 promotes efficient SC destruction at the end of prophase I to ensure faithful inheritance of the genome.
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