Premium
Fundamental cell cycle kinases collaborate to ensure timely destruction of the synaptonemal complex during meiosis
Author(s) -
Argunhan Bilge,
Leung WingKit,
Afshar Negar,
Terentyev Yaroslav,
Subramanian Vijayalakshmi V,
Murayama Yasuto,
Hochwagen Andreas,
Iwasaki Hiroshi,
Tsubouchi Tomomi,
Tsubouchi Hideo
Publication year - 2017
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.15252/embj.201695895
Subject(s) - biology , synaptonemal complex , meiosis , synapsis , microbiology and biotechnology , protein serine threonine kinases , kinase , cell cycle , cell cycle protein , genetics , cell , protein kinase a , gene
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 CDK 1 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 CDK 1 promotes efficient SC destruction at the end of prophase I to ensure faithful inheritance of the genome.