Mitotic Regulation in Aspergillus Nidulans

  1. Joan Marsh
  1. N. Ronald Morris,
  2. Steven W. James and
  3. Matthew J. O'Connell

Published Online: 28 SEP 2007

DOI: 10.1002/9780470514320.ch8

Ciba Foundation Symposium 170 - Regulation of the Eukaryotic Cell Cycle

Ciba Foundation Symposium 170 - Regulation of the Eukaryotic Cell Cycle

How to Cite

Morris, N. R., James, S. W. and O'Connell, M. J. (2007) Mitotic Regulation in Aspergillus Nidulans, in Ciba Foundation Symposium 170 - Regulation of the Eukaryotic Cell Cycle (ed J. Marsh), John Wiley & Sons, Ltd., Chichester, UK. doi: 10.1002/9780470514320.ch8

Author Information

  1. Department of Pharmacology, University of Medicine and Dentistry of New Jersey—Robert W. Johnson Medical School, 675 Hoes Lane, Piscataway, NJ 08854, USA

Publication History

  1. Published Online: 28 SEP 2007

ISBN Information

Print ISBN: 9780471934462

Online ISBN: 9780470514320

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Keywords:

  • mitotic regulation;
  • aspergillus nidulans;
  • DNA replication;
  • chromatin condensation;
  • spindle polymerization

Summary

The nimA and bimE genes of Aspergillus nidulans respectively encode a 79 kDa protein kinase that is a positive regulator of mitosis and a 229 kDa protein that is a negative regulator of mitosis. Either overproduction of nimA or inactivation of bimE can induce mitosis and override the checkpoint associated with incomplete DNA replication. Double mutants between temperature-sensitive nimA and bimE alleles undergo chromatin condensation and spindle polymerization at restrictive temperature, suggesting that the p79nimA kinase is not required for chromatin condensation and spindle polymerization when bimE function is defective. In contrast double mutants carrying ts bimE and nimEcyclinB mutations or bimE and nimTcdC25 mutations are blocked in interphase at restrictive temperature. These results indicate that the mitotic block caused by inactivation of bimE requires activation of the p34cdc2 kinase for chromatin condensation and spindle polymerization to occur. Antibodies against bimE fusion proteins have been used to study p229bimE in wild-type cells and cells overexpressing the bimE gene.