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Fundamental cell cycle kinases collaborate to ensure timely destruction of the synaptonemal complex during meiosis
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- Bilge Argunhan
- Genome Damage and Stability Centre, Life Sciences University of Sussex Brighton, East Sussex UK
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- Wing‐Kit Leung
- Genome Damage and Stability Centre, Life Sciences University of Sussex Brighton, East Sussex UK
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- Negar Afshar
- Genome Damage and Stability Centre, Life Sciences University of Sussex Brighton, East Sussex UK
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- Yaroslav Terentyev
- Genome Damage and Stability Centre, Life Sciences University of Sussex Brighton, East Sussex UK
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- Vijayalakshmi V Subramanian
- Department of Biology New York University New York NY USA
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- Yasuto Murayama
- Institute of Innovative Research Tokyo Institute of Technology Tokyo Japan
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- Andreas Hochwagen
- Department of Biology New York University New York NY USA
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- Hiroshi Iwasaki
- Institute of Innovative Research Tokyo Institute of Technology Tokyo Japan
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- Tomomi Tsubouchi
- Genome Damage and Stability Centre, Life Sciences University of Sussex Brighton, East Sussex UK
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- Hideo Tsubouchi
- Genome Damage and Stability Centre, Life Sciences University of Sussex Brighton, East Sussex UK
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Description
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.
Journal
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- The EMBO Journal
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The EMBO Journal 36 (17), 2488-2509, 2017-07-10
Springer Science and Business Media LLC