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The S. pombe mitotic regulator Cut12 promotes spindle pole body activation and integration into the nuclear envelope

¹ Cancer Research UK Cell Division Group, Paterson Institute for Cancer Research, University of Manchester, Manchester M20 4BX, England, UK
² Research Institute for Disease Mechanism and Control, Nagoya University School of Medicine, Showa-ku, Nagoya 466-8550, Japan
³ Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan

Correspondence to Iain M. Hagan: ihagan{at}picr.man.ac.uk

The fission yeast spindle pole body (SPB) comprises a cytoplasmic structure that is separated from an ill-defined nuclear component by the nuclear envelope. Upon mitotic commitment, the nuclear envelope separating these domains disperses as the two SPBs integrate into a hole that forms in the nuclear envelope. The SPB component Cut12 is linked to cell cycle control, as dominant cut12.s11 mutations suppress the mitotic commitment defect of cdc25.22 cells and elevated Cdc25 levels suppress the monopolar spindle phenotype of cut12.1 loss of function mutations. We show that the cut12.1 monopolar phenotype arises from a failure to activate and integrate the new SPB into the nuclear envelope. The activation of the old SPB was frequently delayed, and its integration into the nuclear envelope was defective, resulting in leakage of the nucleoplasm into the cytoplasm through large gaps in the nuclear envelope. We propose that these activation/integration defects arise from a local deficiency in mitosis-promoting factor activation at the new SPB.

K. Tanaka’s present address is National Institute of Technology and Evaluation, Kisarazu-shi, Chiba 292-0818, Japan.

Abbreviations used in this paper: β-Gal, β-galactosidase; MPF, mitosis-promoting factor; MTOC, microtubule-organizing center; SPB, spindle pole body.

© 2009 Tallada et al.
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