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Telomerase, a protein that maintains telomeres at chromosome ends, is exploited by cancer cells to gain immortality. Researchers are therefore keen to understand how telomerase is regulated. So far, most research has focused on how telomerase is activated but now new work from Kathy Collins and coworkers at the University of California, Berkeley has shown that it is not that simple (Nature Cell Biology). They have found that even when telomerase is active, its action can be restricted by keeping it ‘locked’ away from chromosomes.
Chromosomes duplicate each time a cell divides so that each daughter cell inherits the same number of chromosomes -- a process called ‘replication’. This takes place in the nucleus of the cell. What Collins and colleagues have found is that, in normal cells, telomerase is kept sequestered away from the chromosomes in a subcompartment of the nucleus called the nucleolus, until the time it is needed to ensure proper replication of chromosome ends. So, by restricting the access of telomerase until it is needed, cells presumably prevent any premature action of telomerase on chromosome ends. Importantly, they found that in a variety of cancer cells, telomerase now has continuous access to the chromosomes. Cancer cells are thereby able to bypass the normal regulation of chromosome replication. These findings now open up a new avenue for cancer research: how the movement of telomerase into and out of this compartment is regulated. If we can get a handle on this, we may find a way to prevent cancer cells using it to their advantage. Author contact:
Dr Kathy Collins
Dept of Molecular & Cell Biology
University of California
Berkeley, CA, USA
Tel: +1 510 643 1598
E-mail: kcollins@socrates.berkeley.edu Abstract available online. (C) Nature Cell Biology press release.
Message posted by: Trevor M. D'Souza
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