Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Phosphorylation of the CDK Substrate MSCDK Regulates Synaptonemal Complex Disassembly and Meiosis Metaphase I Transition

Version 1 : Received: 24 April 2023 / Approved: 27 April 2023 / Online: 27 April 2023 (04:55:50 CEST)

How to cite: Li, M.; Zhang, M.; Li, H.; Lu, G.; Chan, W.; Ma, J.; Liu, H.; Huang, T. Phosphorylation of the CDK Substrate MSCDK Regulates Synaptonemal Complex Disassembly and Meiosis Metaphase I Transition. Preprints 2023, 2023041044. https://doi.org/10.20944/preprints202304.1044.v1 Li, M.; Zhang, M.; Li, H.; Lu, G.; Chan, W.; Ma, J.; Liu, H.; Huang, T. Phosphorylation of the CDK Substrate MSCDK Regulates Synaptonemal Complex Disassembly and Meiosis Metaphase I Transition. Preprints 2023, 2023041044. https://doi.org/10.20944/preprints202304.1044.v1

Abstract

Meiosis is a specialized cell division that produces haploid gametes from diploid germ cells, and the phosphorylation activity of cyclin-CDK complexes and Polo-like kinase is required for synaptonemal complex (SC) disassembly and metaphase I exit. Here, we identified a novel protein MSCDK (meiotic substrate of cyclin dependent kinase) that functions as a substrate of CDK1 in initiating SC disassembly and metaphase I transition during meiosis prophase I in mice. Deletion of MSCDK caused germ cell death and infertility in males but not females. Mechanistically, we show that MSCDK is sparsely localized as discrete foci along synaptic homologous chromosomes from the early zygotene to the early diplotene, and we confirm that MSCDK can be phosphorylated by CDK1 and dephosphorylated by the cell cycle exit regulator phosphatase PP1α. We also provide evidence that MSCDK is essential for SC disassembly based on its dephosphorylation-related function, which apparently promotes HSPA2 nuclear recruitment.

Keywords

Meiosis prophase I; Synaptonemal complex (SC) disassembly; Metaphase I transition

Subject

Biology and Life Sciences, Cell and Developmental Biology

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