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Vol. 12, No. 7, pp. 927-942, April 1, 1998
School of Biological Sciences, University of Manchester,
Manchester, M13 9PT UK;
1 Department of Molecular, Cellular,
and Developmental Biology, University of Colorado,
Boulder, Colorado 80309-0347 USA;
2 Imperial Cancer
Research Fund (ICRF), London, WC2A 3PX UK.
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 the
cdc25.22 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.
[Key Words: Mitosis; SPB; cut12; cdc25; MPF; S. pombe]
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