JCB logo
CrossRef
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

Published online 8 September 2003. doi:10.1083/jcb1626rr4
This Article
Right arrow Full Text (PDF, 603K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wells, W. A.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Wells, W. A.
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, 0021-9525/2003/2/961-a $5.00
The Journal of Cell Biology, Volume 162, Number 6, 961-a-961


Research Roundup

A daughter's size is not critical



Only cells with Ace2 (left) repress Cln3 expression in daughters.

Heideman/NAS

The critical size model of cell division is so well established for budding yeast that, as Warren Heideman says, "it's on the wall of the Guinness Brewery." But now Tracy Laabs, Heideman (University of Wisconsin, Madison, WI), and colleagues have found that one of the pillars of the model has an alternative explanation.

The model states that cells only divide once they reach a critical size, which is why smaller daughters delay their division until they reach sizes comparable to those of their mothers. The Madison team found instead that daughters delay thanks to a daughter-localized G1 inhibitor called Ace2.After elimination of Ace2, mothers and daughters divided at the same time, so daughters divided at a smaller size than usual. An Ace2 mutant that was no longer localized to daughters also showed simultaneous division because both mothers and daughters were delayed.

Ace2 works at least in part by controlling levels of the G1 cyclin Cln3. In theory Ace2 could be resetting the critical size in daughters. But, says Heideman, "if you stick with critical size you have so many modifications that you are left with something very cumbersome."

He believes the cell couples growth rate and cell division rate without sensing size. "The critical size model was easily accepted by our minds because it was so elegant," he says, "but it may be hard [for the cell] to engineer." {blacksquare}

Reference:

Laabs, T.L., et al. 2003. Proc. Natl. Acad. Sci. USA. 100:10275–10280.[Abstract/Free Full Text]



William A. Wells

wellsw{at}rockefeller.edu


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
Right arrow Full Text (PDF, 603K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wells, W. A.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Wells, W. A.
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?


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