JCB logo
amgmicro.com
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

Published online 10 February 2003. doi:10.1083/jcb1604rr2
This Article
Right arrow Full Text (PDF, 1392K)
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 LeBrasseur, N.
Right arrow Search for Related Content
PubMed
Right arrow Articles by LeBrasseur, N.
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, 0021-9525/2003/2/464-a $5.00
The Journal of Cell Biology, Volume 160, Number 4, 464-a-465


Research Roundup

Rec'd and repaired


The structures of replicating DNAs change (left to right) to allow repair work.

Courcelle/AAAS

DNA replication stalls when the polymerase encounters lesions in the DNA, but recovers soon after lesion repair. In a recent work, Justin Courcelle and colleagues (Mississippi State University, Mississippi State, MS) examine what happens to the replication fork during this downtime. The results show that maintaining the correct fork structure depends on recombination proteins that may help to prevent illegitimate strand exchanges.

Courcelle's group used two-dimensional gel electrophoresis to examine the shapes of a replicating bacterial plasmid. Advancing replication forks yielded the expected Y-shaped structure. But UV-induced lesions stalled the replication fork and produced X-shaped structures. These structures represent the nascent DNA backing up from the apex of a Y-shaped fork. The stalled structures were processed by RecQ and RecJ and maintained by RecA and RecF, which are the same proteins that promote homologous DNA pairing during recombinational processes.

A mid-replication stall is "like catching a cell with its pants down," according to Courcelle. "It can't live as one and a half cells for eternity," he says. Unchecked free DNA ends are recombinogenic. Fork stabilization by these Rec proteins may be essential for preventing unwanted mitotic recombination and its potentially cancerous consequences. In addition, fork regression and Rec binding probably delays replication long enough for repair enzymes or SOS polymerases either to repair the lesion or to replicate past it. Whether RecA and RecF recruit repair enzymes or simply maintain an open fork remains to be determined. {blacksquare}

Reference:

Courcelle, J., et al. 2003. Science. 10.1126/science.1081328.



Nicole LeBrasseur

lebrasn{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, 1392K)
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 LeBrasseur, N.
Right arrow Search for Related Content
PubMed
Right arrow Articles by LeBrasseur, N.
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