BUB-1 and CENP-C recruit PLK-1 to control chromosome alignment and segregation during meiosis I in C. elegans oocytes.
BUB-1 and CENP-C recruit PLK-1 to control chromosome alignment and segregation during meiosis I in C. elegans oocytes.
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DOI：
10.7554/elife.84057
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发表时间：
2023-04-17
期刊：
影响因子：
7.7
通讯作者：
Pelisch F
中科院分区：
文献类型：
--
作者：
Taylor SJP;Bel Borja L;Soubigou F;Houston J;Cheerambathur DK;Pelisch F
磷酸化是一种关键的翻译后修饰，在许多生物学过程中用于快速和可逆地调节蛋白质定位和活性。Polo样激酶1（PLK-1）是有丝分裂和减数分裂细胞分裂所必需的，其关键功能在真核生物中是保守的。PLK-1在有丝分裂过程中的作用和调节已得到很好的表征。然而，PLK-1在减数分裂过程中的独立作用和调控仍然不清楚。在这里，我们使用秀丽隐杆线虫卵母细胞显示PLK-1在减数分裂纺锤体组装和/或稳定性，染色体排列和分离，以及减数分裂I期间的极体挤出中发挥独特的作用。此外，通过活体成像和生化分析的结合，我们确定了PLK-1在C.卵母细胞减数分裂。纺锤体组装检查点激酶BUB-1直接将PLK-1募集到动粒和中间二价体，而PLK-1的染色体臂群体依赖于与着丝粒相关蛋白CENP-CHCP-4的直接相互作用。我们发现，干扰BUB-1和CENP-CHCP-4对PLK-1的募集导致严重的减数分裂缺陷，导致高度非整倍体的卵母细胞。总之，我们的研究结果揭示了PLK-1在卵母细胞减数分裂过程中所起的作用，并提供了PLK-1靶向减数分裂染色体的机制理解。
Phosphorylation is a key post-translational modification that is utilised in many biological processes for the rapid and reversible regulation of protein localisation and activity. Polo-like kinase 1 (PLK-1) is essential for both mitotic and meiotic cell divisions, with key functions being conserved in eukaryotes. The roles and regulation of PLK-1 during mitosis have been well characterised. However, the discrete roles and regulation of PLK-1 during meiosis have remained obscure. Here, we used Caenorhabditis elegans oocytes to show that PLK-1 plays distinct roles in meiotic spindle assembly and/or stability, chromosome alignment and segregation, and polar body extrusion during meiosis I. Furthermore, by a combination of live imaging and biochemical analysis we identified the chromosomal recruitment mechanisms of PLK-1 during C. elegans oocyte meiosis. The spindle assembly checkpoint kinase BUB-1 directly recruits PLK-1 to the kinetochore and midbivalent while the chromosome arm population of PLK-1 depends on a direct interaction with the centromeric-associated protein CENP-CHCP-4. We found that perturbing both BUB-1 and CENP-CHCP-4 recruitment of PLK-1 leads to severe meiotic defects, resulting in highly aneuploid oocytes. Overall, our results shed light on the roles played by PLK-1 during oocyte meiosis and provide a mechanistic understanding of PLK-1 targeting to meiotic chromosomes.