JCB logo
Accuri Cytometers
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 668K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Carroll, C. W.
Right arrow Articles by Kellogg, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Carroll, C. W.
Right arrow Articles by Kellogg, D.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

© The Rockefeller University Press, 0021-9525/1998//709 $5.00
The Journal of Cell Biology, Volume 143, Number 3, , 1998 709-717

Regular Articles

The Septins Are Required for the Mitosis-specific Activation of the Gin4 Kinase



Christopher W. Carroll, Roger Altman, David Schieltz{ddagger}, John R. Yates, III{ddagger}, and Douglas Kellogg

Department of Biology, Sinsheimer Laboratories, University of California, Santa Cruz, California 95064; and {ddagger} Center for Comprehensive Biology, University of Washington, Seattle, Washington 98195-7730

In budding yeast, a protein kinase called Gin4 is specifically activated during mitosis and functions in a pathway initiated by the Clb2 cyclin to control bud growth. We have used genetics and biochemistry to identify additional proteins that function with Gin4 in this pathway, and both of these approaches have identified members of the septin family. Loss of septin function produces a phenotype that is very similar to the phenotype caused by loss of Gin4 function, and the septins are required early in mitosis to activate Gin4 kinase activity. Furthermore, septin mutants display a prolonged mitotic delay at the short spindle stage, consistent with a role for the septins in the control of mitotic events. Members of the septin family bind directly to Gin4, demonstrating that the functions of Gin4 and the septins must be closely linked within the cell. These results demonstrate that the septins in budding yeast play an integral role in the mitosis-specific regulation of the Gin4 kinase and that they carry out functions early in mitosis.

Key Words: septins • Gin4 • cyclin-dependent kinase • mitosis • morphogenesis

Abbreviations used in this paper: GST, glutathione-S-transferase; ORF, open reading frame.

Address all correspondence to Douglas Kellogg, Department of Biology, Sinsheimer Laboratories, University of California, Santa Cruz, CA 95064. Tel.: (831) 459-5659. Fax: (831) 459-3139. E-mail: kellogg{at}darwin.ucsc.edu

C.W. Carroll's and R. Altman's present address is Department of Biochemistry and Biophysics, University of California, San Francisco, CA 94143.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?


This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents