Fundamental cell cycle kinases collaborate to ensure timely destruction of the synaptonemal complex during meiosis
| Autor: | Yaroslav Terentyev, Vijayalakshmi V. Subramanian, Tomomi Tsubouchi, Bilge Argunhan, Negar Afshar, Hiroshi Iwasaki, Andreas Hochwagen, Wing Kit Leung, Hideo Tsubouchi, Yasuto Murayama |
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| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Dbf4‐dependent Cdc7 kinase Mitotic crossover RAD51 Cell Cycle Proteins homologous recombination Biology General Biochemistry Genetics and Molecular Biology Fungal Proteins 03 medical and health sciences Meiotic Prophase I Meiosis Homologous chromosome meiosis Phosphorylation Molecular Biology Features Cyclin-dependent kinase 1 General Immunology and Microbiology General Neuroscience synaptonemal complex Articles Cell cycle Molecular biology Cell biology Synaptonemal complex enzymes and coenzymes (carbohydrates) 030104 developmental biology Saccharomycetales Protein Kinases Polo‐like kinase |
| Zdroj: | The EMBO Journal. 36(No. 17):2488-2509 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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