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© The Rockefeller University Press, 0021-9525/1997//119 $5.00
The Journal of Cell Biology, Volume 138, Number 1, , 1997 119-130

Article

Control of Mitotic Events by Nap1 and the Gin4 Kinase



Roger Altman and Douglas Kellogg

Sinsheimer Laboratories, Department of Biology, University of California, Santa Cruz, California 95064

Little is known about the pathways used by cyclins and cyclin-dependent kinases to induce the events of the cell cycle. In budding yeast, a protein called Nap1 binds to the mitotic cyclin Clb2, and Nap1 is required for the ability of Clb2 to induce specific mitotic events, but the role played by Nap1 is unclear. We have used genetic and biochemical approaches to identify additional proteins that function with Nap1 in the control of mitotic events. These approaches have both identified a protein kinase called Gin4 that is required for the ability of Clb2 and Nap1 to promote the switch from polar to isotropic bud growth that normally occurs during mitosis. Gin4 is also required for the ability of Clb2 and Nap1 to promote normal progression through mitosis. The Gin4 protein becomes phosphorylated as cells enter mitosis, resulting in the activation of Gin4 kinase activity, and the phosphorylation of Gin4 is dependent upon Nap1 and Clb2 in vivo. Affinity chromatography experiments demonstrate that Gin4 binds tightly to Nap1, indicating that the functions of these two proteins are closely tied within the cell. These results demonstrate that the activation of Gin4 is under the control of Clb2 and Nap1, and they provide an important step towards elucidating the molecular pathways that link cyclin-dependent kinases to the events they control.

1. Abbreviation used in this paper: YPD, yeast/peptone/dextrose.

The initial stages of the genetic screen for mutants in bud growth control were carried out by D. Kellogg while working as a postdoctoral researcher in the lab of A. Murray, who also provided helpful advice and comments on the manuscript. We thank Y. Jin and A. Chisholm for use of their microscope, and we thank C. Wilson for use of his DNA synthesizer. We also thank A. Straight, K. Hardwick, D. Morgan, B. Sullivan, L. Wang, A. Kashyap, Z. Zimmerman, and A. Sreenivasan for helpful advice regarding these experiments, and/or critical reading of the manuscript.

Please address all correspondence to Douglas Kellogg, Sinsheimer Laboratories, Department of Biology, University of California at Santa Cruz, Santa Cruz, CA 95064. Tel.: (408) 459-5659. Fax: (408) 459-3139. e-mail: kellogg{at}darwin.ucsc.edu


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