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

Published online
doi:10.1083/jcb.1811rr1
The Journal of Cell Biology, Vol. 181, No. 1, 5-
The Rockefeller University Press, 0021-9525 $30.00
© LeBrasseur
This Article
Right arrow Full Text (PDF, 883K)
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?

Research Roundup

Stem cells sport longest telomeres


Adult stem cell hideouts can be identified by the presence of extra long telomeres, according to findings from Ignacio Flores, Maria Blasco (Spanish National Cancer Center, Madrid, Spain), and colleagues.

Because of their location at chromosome tips, telomeres shorten with every cell division. Stem cells divide more slowly than other cell types, so Blasco's group reasoned that they might have the longest telomeres. Using a precise, quantitative version of FISH with telomere sequences, the group found that cells with the longest telomeres corresponded to known stem cell niches in skin, brain, testis, and other tissues.

The approach bypasses the need to identify distinguishing stem cell markers in each tissue type. Until now, the only other generally applicable method was the slower label-retaining technique. The authors will now test other tissues to identify unknown stem cell populations or resolve controversial ones.

Telomeres in the stem cell niches and elsewhere were dramatically shorter in two-year-old mice than in those just a year younger. The group hypothesizes that telomere maintenance mechanisms may go awry in old age. If stem cells with stubby telomeres are unable to function normally, this shortening may be a cause of aging. The group would now like to try to extend lifespan in mice by delaying telomere shortening. Formula

Reference:

Flores, I., et al. 2008. Genes Dev. 22:654–667.[Abstract/Free Full Text]



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, 883K)
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