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激酶PLK1在雄性小鼠减数分裂的终变期/中期I转换过程中调节侧生元件的解体和着丝粒内部的组装。

Kinase PLK1 regulates the disassembly of the lateral elements and the assembly of the inner centromere during the diakinesis/metaphase I transition in male mouse meiosis.

作者信息

Gómez Rocío, Viera Alberto, Moreno-Mármol Tania, Berenguer Inés, Guajardo-Grence Andrea, Tóth Attila, Parra María Teresa, Suja José A

机构信息

Unidad de Biología Celular, Departamento de Biología, Facultad de Ciencias, Universidad Autónoma de Madrid, Madrid, Spain.

Departamento de Neuropatología Molecular, Centro de Biología Molecular Severo Ochoa, Campus de la Universidad Autónoma de Madrid, Madrid, Spain.

出版信息

Front Cell Dev Biol. 2023 Jan 13;10:1069946. doi: 10.3389/fcell.2022.1069946. eCollection 2022.

Abstract

PLK1 is a serine/threonine kinase with crucial roles during mitosis. However, its involvement during mammalian male meiosis remains largely unexplored. By inhibiting the kinase activity of PLK1 using BI 2536 on organotypic cultures of seminiferous tubules, we found that the disassembly of SYCP3 and HORMAD1 from the lateral elements of the synaptonemal complex during diakinesis is impeded. We also found that the normal recruitment of SYCP3 and HORMAD1 to the inner centromere in prometaphase I spermatocytes did not occur. Additionally, we analyzed the participation of PLK1 in the assembly of the inner centromere by studying its implication in the Bub1-H2AT120ph-dependent recruitment of shugoshin SGO2, and the Haspin-H3T3ph-dependent recruitment of Aurora B/C and Borealin. Our results indicated that both pathways are regulated by PLK1. Altogether, our results demonstrate that PLK1 is a master regulator of the late prophase I/metaphase I transition in mouse spermatocytes.

摘要

PLK1是一种丝氨酸/苏氨酸激酶,在有丝分裂过程中发挥关键作用。然而,其在哺乳动物雄性减数分裂中的作用在很大程度上仍未得到探索。通过在生精小管的器官型培养物中使用BI 2536抑制PLK1的激酶活性,我们发现终变期期间SYCP3和HORMAD1从联会复合体侧元件上的解离受到阻碍。我们还发现,在前期I精母细胞中,SYCP3和HORMAD1正常向内着丝粒的募集未发生。此外,我们通过研究PLK1在Bub1-H2AT120ph依赖性的守护蛋白SGO2募集以及Haspin-H3T3ph依赖性的极光激酶B/C和Borealin募集中的作用,分析了PLK1在内着丝粒组装中的参与情况。我们的结果表明,这两条途径均受PLK1调控。总之,我们的结果表明PLK1是小鼠精母细胞前期I晚期/中期I转换的主要调节因子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/474a/9887526/95d6bb03c620/fcell-10-1069946-g001.jpg

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