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© The Rockefeller University Press, 0021-9525/1997//969 $5.00
The Journal of Cell Biology, Volume 136, Number 5, , 1997 969-982

Article

The Yeast CDC37 Gene Interacts with MPS1 and Is Required for Proper Execution of Spindle Pole Body Duplication



Amy R. Schutz, Thomas H. Giddings, Jr., Estelle Steiner, and Mark Winey

Department of Molecular, Cellular, and Developmental Biology, University of Colorado–Boulder, Boulder, Colorado 80309-0347

The MPS1 gene from Saccharomyces cerevisiae encodes an essential protein kinase required for spindle pole body (SPB) duplication and for the mitotic spindle assembly checkpoint. Cells with the mps1-1 mutation fail early in SPB duplication and proceed through monopolar mitosis with lethal consequences. We identified CDC37 as a multicopy suppressor of mps1-1 temperature-sensitive growth. Suppression is allele specific, and synthetic lethal interactions occur between mps1 and cdc37 alleles. We examined the cdc37-1 phenotype for defects related to the SPB cycle. The cdc37-1 temperature-sensitive allele causes unbudded, G1 arrest at Start (Reed, S.I. 1980. Genetics. 95: 561–577). Reciprocal shifts demonstrate that cdc37-1 arrest is interdependent with {alpha}-factor arrest but is not a normal Start arrest. Although the cells are responsive to {alpha}-factor at the arrest, SPB duplication is uncoupled from other aspects of G1 progression and proceeds past the satellite-bearing SPB stage normally seen at Start. Electron microscopy reveals side-by-side SPBs at cdc37-1 arrest. The outer plaque of one SPB is missing or reduced, while the other is normal. Using the mps2-1 mutation to distinguish between the SPBs, we find that the outer plaque defect is specific to the new SPB. This phenotype may arise in part from reduced Mps1p function: although Mps1p protein levels are unaffected by the cdc37-1 mutation, kinase activity is markedly reduced. These data demonstrate a requirement for CDC37 in SPB duplication and suggest a role for this gene in G1 control. CDC37 may provide a chaperone function that promotes the activity of protein kinases.

Abbreviations used in this paper: 5-FOA, 5-fluoro-orotic acid; cdc, cell division cycle; DIG, digoxigenin; ORF, open reading frame; ProA, protein A; SMO1, suppressor of mps one; SPB, spindle pole body; ts, temperature sensitive for growth.

This work was initiated under an American Cancer Society grant (MV63940) and completed with support from the National Institutes of Health (NIH GM51312). Additional support was from an American Cancer Society JFRA (A70760) and the Pew Scholars Program in the Biomedical Sciences award (P0020SC) to M. Winey. An NIH Training Grant (GM07135) supported A.R. Schutz and E. Steiner. Further support for A.R. Schutz was provided by a National Science Foundation Predoctoral Fellowship and Truman Scholarship, and for E. Steiner by the Achievement Rewards for College Scientists Foundation.

Address all correspondence to Mark Winey, Department of Molecular, Cellular, and Developmental Biology, University of Colorado–Boulder, Boulder, CO 80309-0347. Tel.: (303) 492-3409. Fax: (303) 492-7744. E-mail: Mark.Winey{at}Colorado.edu


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