BIMA(APC3), component of the Aspergillus anaphase promoting complex/cyclosome, is required for a G2 checkpoint blocking entry into mitosis in the absence of NIMA function

C. Mark Lies, Jijun Cheng, Steven W. James, N. Ronald Morris, Matthew J. O'Connell, P. M. Mirabito

Research output: Contribution to journalArticlepeer-review

19 Scopus citations

Abstract

Temperature sensitive (ts) nimA mutants of Aspergillus nidulans arrest at a unique point in G2 which is post activation of CDC2. Here we show that this G2 arrest is due to loss of nimA function and that it is dependent on BIMA(APC3), a component of the anaphase promoting complex/cyclosome (APC/C). Whereas nimA single mutants arrested in G2 with decondensed chromatin and interphase microtubule arrays, nimA, bimA(APC3) double mutants arrested growth with condensed chromatin and aster-like microtubule arrays. nimA, bimA(APC3) double mutants entered mitosis with kinetics similar to bimA(APC3) single mutants and wild-type cells, indicating a checkpoint-like role for BIMA(APC3) in G2. Even cells which had been depleted for NIMA protein and which contained insignificant levels of NIMA kinase activity entered mitosis on inactivation of bimA(APC3). BIMA(APC3) was present in a > 25S complex containing BIME(APC1), and bimA(APC3) mutants were sensitive to elevated CYCLIN B expression, consistent with BIMA(APC3) being a component of the APC/C. Inactivation of bimA(APC3) had little affect on the steady state levels of the B-type cyclin, NIME(Cyclin B). Our results indicate that BIMA(APC3), and most likely the APC/C itself, is activated in G2 in nimA mutants. We propose that APC/C activation is part of a novel, late G2 checkpoint, which responds to a defective process or structure in nimA mutants, and which prevents inappropriate entry into mitosis.

Original languageEnglish
Pages (from-to)1453-1465
Number of pages13
JournalJournal of Cell Science
Volume111
Issue number10
StatePublished - 1998

Keywords

  • APC
  • Checkpoint
  • Cyclosome
  • NIMA

ASJC Scopus subject areas

  • Cell Biology

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