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γ-微管蛋白在 G1-S 交界处使 APC/C(Cdh1)失活中起着关键作用。

γ-Tubulin plays a key role in inactivating APC/C(Cdh1) at the G(1)-S boundary.

机构信息

Department of Molecular Biosciences, University of Kansas, Lawrence, KS 66045, USA.

出版信息

J Cell Biol. 2012 Sep 3;198(5):785-91. doi: 10.1083/jcb.201203115. Epub 2012 Aug 27.

Abstract

A γ-tubulin mutation in Aspergillus nidulans, mipA-D159, causes failure of inactivation of the anaphase-promoting complex/cyclosome (APC/C) in interphase, resulting in failure of cyclin B (CB) accumulation and removal of nuclei from the cell cycle. We have investigated the role of CdhA, the A. nidulans homologue of the APC/C activator protein Cdh1, in γ-tubulin-dependent inactivation of the APC/C. CdhA was not essential, but it targeted CB for destruction in G(1), and APC/C(CdhA) had to be inactivated for the G(1)-S transition. mipA-D159 altered the localization pattern of CdhA, and deletion of the gene encoding CdhA allowed CB to accumulate in all nuclei in strains carrying mipA-D159. These data indicate that mipA-D159 causes a failure of inactivation of APC/C(CdhA) at G(1)-S, perhaps by altering its localization to the spindle pole body, and, thus, that γ-tubulin plays an important role in inactivating APC/C(CdhA) at this point in the cell cycle.

摘要

在构巢曲霉中,γ-微管蛋白突变 mipA-D159 导致后期促进复合物/环体(APC/C)在间期失活失败,从而导致细胞周期中细胞周期蛋白 B(CB)积累和细胞核从细胞周期中去除失败。我们研究了 CdhA(APC/C 激活蛋白 Cdh1 的构巢曲霉同源物)在 γ-微管蛋白依赖性 APC/C 失活中的作用。CdhA 不是必需的,但它在 G1 期靶向 CB 进行破坏,并且 APC/C(CdhA)必须失活才能进行 G1-S 转换。mipA-D159 改变了 CdhA 的定位模式,并且在携带 mipA-D159 的菌株中删除编码 CdhA 的基因允许 CB 在所有核中积累。这些数据表明,mipA-D159 导致 APC/C(CdhA)在 G1-S 时失活失败,可能是通过改变其向纺锤体极体的定位,因此,γ-微管蛋白在细胞周期的这一点上在 APC/C(CdhA)失活中发挥重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ec6/3432763/92e5bdf564d3/JCB_201203115R_Fig1.jpg

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