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Abstract

During meiosis, accurate coordination of the completion of homologous recombination and synaptonemal complex {(SC)} disassembly during the prophase to metaphase I {(G2/MI)} transition is essential to avoid aneuploid gametes and infertility. Previous studies have shown that kinase activity is required to promote meiotic prophase exit. The first step of the {G2/MI} transition is the disassembly of the central element components of the {SC;} however, the kinase(s) required to trigger this process remains unknown. Here we assess roles of polo-like kinases {(PLKs)} in mouse spermatocytes, both in vivo and during prophase exit induced ex vivo by the phosphatase inhibitor okadaic acid. All four {PLKs} are expressed during the first wave of spermatogenesis. Only {PLK1} (not {PLK2-4)} localizes to the {SC} during the {G2/MI} transition. The {SC} central element proteins {SYCP1,} {TEX12} and {SYCE1} are phosphorylated during the {G2/MI} transition. However, treatment of pachytene spermatocytes with the {PLK} inhibitor {BI} 2536 prevented the okadaic-acid-induced meiotic prophase exit and inhibited phosphorylation of the central element proteins as well as their removal from the {SC.} Phosphorylation assays in vitro demonstrated that {PLK1,} but not {PLK2-4,} phosphorylates central element proteins {SYCP1} and {TEX12.} These findings provide mechanistic details of the first stage of {SC} disassembly in mammalian spermatocytes, and reveal that {PLK-mediated} phosphorylation of central element proteins is required for meiotic prophase exit.

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Jordan, P. W., Karppinen, J., & Handel, M. A. (2012). Polo-like kinase is required for synaptonemal complex disassembly and phosphorylation in mouse spermatocytes. Journal of Cell Science, 125(21), 5061–5072. https://doi.org/10.1242/jcs.105015

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