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

This Article Full Text (PDF, 249K) PPT slides of all figures Alert me when this article is cited Services Email this article Similar articles in this journal Alert me to new content in the JCB Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by LeBrasseur, N. Search for Related Content PubMed Articles by LeBrasseur, N. Social Bookmarking                            What's this?

© The Rockefeller University Press, 0021-9525/2002/9/1154 $5.00
The Journal of Cell Biology, Volume 158, Number 7, September 30, 2002 1154-1154

Hiding telomerase from chromatin

Telomerase (green) escapes the nucleoli (red) in cancer cells (bottom). Collins/Macmillan

Telomerase helps cancerous cells survive by extending telomeres at the end of chromosomes. According to new results from Judy Wong, Leonard Kusdra, and Kathleen Collins (University of California, Berkeley, CA), cancer cells recruit additional telomerase by setting it free from its subnuclear storage depot.

Telomerase is activated upon association of two subunits, telomerase reverse transcriptase (TERT) and telomerase RNA, into a ribonucleoprotein (RNP) complex. Collins' group tracked the active form in normal and cancerous cells by expressing GFP-labeled TERT in limiting amounts that would assemble rapidly with the RNP. This technique revealed that telomerase differed mainly in its location. "A normal cell hides telomerase, by tying it to the nucleolus," says Collins. In these cells, telomerase was concentrated in the nucleoplasm during S phase, when its activity is required to maintain chromosome ends. In contrast, transformed cells released all of their telomerase from the nucleoli, regardless of cell cycle phase.

The proteins that control telomerase localization are not yet known, but the ability of transformed cells to bypass this regulation may give them a twofold advantage. First, telomerase would be more effective on an established telomere because more of it is released from nucleolar stores. Additionally, continuous release of telomerase may support the high genomic instability of cancerous cells: adding telomeres to broken chromosome ends might allow normal segregation of rearranged chromosomes that might otherwise arrest the cell cycle.

Reference:

Wong, J.M.Y., et al. 2002. Nat. Cell Biol. 4:731–736.[CrossRef][Medline]

Nicole LeBrasseur

lebrasn{at}rockefeller.edu

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

This Article Full Text (PDF, 249K) PPT slides of all figures Alert me when this article is cited Services Email this article Similar articles in this journal Alert me to new content in the JCB Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by LeBrasseur, N. Search for Related Content PubMed Articles by LeBrasseur, N. Social Bookmarking                            What's this?