JCB logo
Avanti Polar Lipids, Inc.
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

Published online 4 October 2004. doi:10.1083/jcb1671rr3
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 167, Number 1, 15-15
This Article
Right arrow Full Text (PDF, 530K)
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?

Research Roundup

Flow to the front



Myosin flows to the anterior, taking PAR proteins with it.

MUNRO/ELSEVIER

Cortical actomyosin flow carries polarity proteins to the front of the worm embryo, according to Edwin Munro (Center for Cell Dynamics, Friday Harbor, WA), Jeremy Nance, and James Priess (Fred Hutchinson Cancer Research Center, Seattle, WA). Similar flows may set up polarity in many other systems.

The idea that asymmetrical contraction drives cortical flow and the segregation of cell fate determinants has a long and controversial history. Earlier efforts were dogged by the transience of the flow and different results after the use of different fixation methods.

But when Munro finally had GFP-labeled myosin to work with, "the whole story unfolded in front of me," he says. Contractile, coupled foci of cortical myosin gave way at the posterior when the sperm centrosomes approached the posterior cortex. The actomyosin network then contracted toward the anterior, taking a host of cytoskeletal proteins and anterior determinants with it.

Absence of these anterior determinants allows the PAR-2 determinant to attach to the posterior cortex, where it was needed to prevent a reverse flow of actomyosin back to the posterior. Both the PAR-2 and centrosome signal may somehow weaken or degrade parts of the actomyosin system, although the specific mechanism is a mystery.

Similar flows were seen at the 8-cell stage when cells set up PAR-based apicobasal polarity. In this case, the cue that weakens the actomyosin cortex may be basolateral contact with surrounding cells. "Any time you get differences in contractility you'll see flows in the cortex," says Munro. "The mystery is not why do you have flows but how do you prevent flows." {rr_end}

Reference:

Munro, E., et al. 2004. Dev. Cell. 7:413–424.[CrossRef][Medline]



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, 530K)
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