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有序组装为酵母中心体复制周期中的固有不对称性提供了基础，这需要细胞周期蛋白依赖性激酶。

Orderly assembly underpinning built-in asymmetry in the yeast centrosome duplication cycle requires cyclin-dependent kinase.

机构信息

Department of Genetics, University of Cambridge, Cambridge, United Kingdom.

Stowers Institute for Medical Research, Kansas City, United States.

出版信息

Elife. 2020 Aug 27;9:e59222. doi: 10.7554/eLife.59222.

DOI:10.7554/eLife.59222
PMID:32851976
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7470843/
Abstract

Asymmetric astral microtubule organization drives the polarized orientation of the mitotic spindle and primes the invariant inheritance of the old spindle pole body (SPB, the yeast centrosome) by the bud. This model has anticipated analogous centrosome asymmetries featured in self-renewing stem cell divisions. We previously implicated Spc72, the cytoplasmic receptor for the gamma-tubulin nucleation complex, as the most upstream determinant linking SPB age, functional asymmetry and fate. Here we used structured illumination microscopy and biochemical analysis to explore the asymmetric landscape of nucleation sites inherently built into the spindle pathway and under the control of cyclin-dependent kinase (CDK). We show that CDK enforces Spc72 asymmetric docking by phosphorylating Nud1/centriolin. Furthermore, CDK-imposed order in the construction of the new SPB promotes the correct balance of nucleation sites between the nuclear and cytoplasmic faces of the SPB. Together these contributions by CDK inherently link correct SPB morphogenesis, age and fate.

摘要

不对称的星体微管组织驱动有丝分裂纺锤体的极化取向，并通过芽将旧纺锤体极体（SPB，酵母中心体）的不变遗传物质进行预编程。该模型预测了自我更新的干细胞分裂中类似的中心体不对称性。我们之前曾表明，γ-微管核形成复合物的细胞质受体 Spc72 是连接 SPB 年龄、功能不对称性和命运的最上游决定因素。在这里，我们使用结构照明显微镜和生化分析来探索固有的核形成位点在纺锤体途径中的不对称景观，以及它们受细胞周期蛋白依赖性激酶（CDK）的控制。我们表明，CDK 通过磷酸化 Nud1/中心粒蛋白来强制 Spc72 不对称对接。此外，CDK 对新 SPB 构建的有序性促进了核和质膜面之间 SPB 核形成位点的正确平衡。这些由 CDK 产生的贡献本质上连接了正确的 SPB 形态发生、年龄和命运。

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Ser/Thr protein phosphatases in fungi: structure, regulation and function.真菌中的丝氨酸/苏氨酸蛋白磷酸酶：结构、调控与功能
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