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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BUB-1 和 CENP-C 招募 PLK-1 来控制线虫卵母细胞减数分裂 I 期间的染色体排列和分离
DOI：
10.1101/2022.10.07.511262
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发表时间：
2022
期刊：
影响因子：
--
通讯作者：
Taylor S
中科院分区：
文献类型：
--
作者：
Taylor S
磷酸化是一种关键的翻译后修饰，在许多生物过程中被用来快速和可逆地调节蛋白质的定位和活性。Polo-like kinase1(PLK-1)在有丝分裂和减数分裂过程中都是必不可少的，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控已经被很好地描述了。然而，PLK-1在减数分裂过程中的离散作用和调控仍然不清楚。在此，我们以线虫卵母细胞为研究对象，研究了PLK-1在线虫卵母细胞减数分裂过程中对纺锤体的组装和/或稳定性、染色体的排列和分离以及极体排出等方面的作用。此外，结合活体成像和生化分析，我们确定了线虫卵母细胞减数分裂过程中PLK-1的染色体募集机制。纺锤体组装检查点激酶bub-1直接将PLK-1招募到着丝粒和中二价体，而PLK-1的染色体臂群体依赖于与着丝粒相关蛋白CENP-C HCP-4的直接相互作用。我们发现，干扰BUB-1和CENP-C HCP-4对PLK-1的招募会导致严重的减数分裂缺陷，导致高度非整倍体的卵母细胞。总体而言，我们的结果阐明了PLK-1在卵母细胞减数分裂中所扮演的角色，并提供了对PLK-1靶向减数分裂染色体的机制的理解。
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-C HCP-4. We found that perturbing both BUB-1 and CENP-C HCP-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.
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