γ-Tubulin plays a key role in inactivating APC/CCdh1 at the G1-S boundary

Heather Edgerton-Morgan, Berl R. Oakley

Research output: Contribution to journalArticlepeer-review

18 Scopus citations

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 G1, and APC/CCdhA had to be inactivated for the G1-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/CCdhA at G1-S, perhaps by altering its localization to the spindle pole body, and, thus, that γ-tubulin plays an important role in inactivating APC/CCdhA at this point in the cell cycle.

Original languageEnglish (US)
Pages (from-to)785-791
Number of pages7
JournalJournal of Cell Biology
Volume198
Issue number5
DOIs
StatePublished - Sep 2012
Externally publishedYes

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