4.7 Article

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

Journal

JOURNAL OF CELL BIOLOGY
Volume 198, Issue 5, Pages 785-791

Publisher

ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201203115

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Funding

  1. National Institutes of Health [GM031837]
  2. University of Kansas Endowment

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A gamma-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 gamma-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 gamma-tubulin plays an important role in inactivating APC/C-CdhA at this point in the cell cycle.

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