The fission yeast SPB component Cut12 links bipolar spindle formation to mitotic control

  1. Alan J. Bridge,
  2. Mary Morphew,
  3. Rachel Bartlett, and
  4. Iain M. Hagan
  1. School of Biological Sciences, University of Manchester, Manchester, M13 9PT UK; Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder, Colorado 80309-0347 USA; Imperial Cancer Research Fund (ICRF), London, WC2A 3PX UK.

Abstract

During fission yeast mitosis, the duplicated spindle pole bodies (SPBs) nucleate microtubule arrays that interdigitate to form the mitotic spindle. cut12.1 mutants form a monopolar mitotic spindle, chromosome segregation fails, and the mutant undergoes a lethal cytokinesis. The cut12 + gene encodes a novel 62-kD protein with two predicted coiled coil regions, and one consensus phosphorylation site for p34cdc2 and two for MAP kinase. Cut12 is localized to the SPB throughout the cell cycle, predominantly around the inner face of the interphase SPB, adjacent to the nucleus. cut12 + is allelic to stf1 +;stf1.1 is a gain-of-function mutation bypassing the requirement for the Cdc25 tyrosine phosphatase, which normally dephosphorylates and activates the p34cdc2/cyclin B kinase to promote the onset of mitosis. Expressing a cut12 + cDNA carrying the stf1.1 mutation also suppressed cdc25.22.The spindle defect in cut12.1 is exacerbated by thecdc25.22 mutation, and stf1.1 cells formed defective spindles in a cdc25.22 background at high temperatures. We propose that Cut12 may be a regulator or substrate of the p34cdc2 mitotic kinase.

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Footnotes

  • Corresponding author.

  • E-MAIL Iain.Hagan{at}man.ac.uk; FAX 44 161 275 5082.

    • Received August 29, 1997.
    • Accepted February 4, 1998.
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