Department of Molecular Biosciences, University of Kansas, Lawrence, KS 66045, USA.
J Cell Biol. 2012 Sep 3;198(5):785-91. doi: 10.1083/jcb.201203115. Epub 2012 Aug 27.
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.
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。
