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
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
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Keywords
Details 詳細情報について
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- CRID
- 1360002219688824960
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- NII Article ID
- 120007117670
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- ISSN
- 14602075
- 15514005
- 02614189
- 15384101
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- Data Source
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- Crossref
- CiNii Articles
- KAKEN
- OpenAIRE