Long Live Rat Cells

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Human cells, extracted from the body and grown in a culture dish, don't divide forever. With every division, their telomeres--the ends of their chromosomes--get shorter, providing a molecular clock of sorts that stops their growth after a defined number of doublings. This phenomenon is termed "replicative senescence" and prevents cells from accumulating too many genetic mutations that may turn them into cancer cells. Rat and mouse cells do not feature such a "countdown" mechanism, and researchers from London have now shown that at least some types of rat cells from the nervous system can divide virtually forever without turning cancerous.

Until now, it had been a riddle to many researchers as to why cultured rodent cells did stop dividing, despite the fact that they have an enzyme called telomerase, which keeps their telomeres at a constant length. But the reason, as it turns out, is probably that these cells were kept under the wrong conditions. Two groups from University College London, led by Alison Lloyd and Martin Raff, report in ScienceExpress today that glial cells and oligodendrocyte precursor cells, both removed from the central nervous system of young rats, can divide indefinitely--in one case for more than 20 months--if the culture medium contains or lacks certain ingredients, such as hormones. Unlike cancer cells, though, which also grow forever but are unstoppable, these cells still stop dividing if, for example, they get damaged by x-rays.

Why do human cells have an built-in "division clock" that some rat cells seem to lack? Humans are larger and live longer than rats. It is more likely that one of their many cells, over a life time, will acquire enough mutations to turn into a cancer cell. One way to prevent this malignant transition is to limit the number of cell divisions. In a rat, this safety measure might not be necessary.

Do the telomeres in cancer cells get shorter each time the cell divides?, Scientific American, January 2001. Turning Back the Strands of Time, Scientific American, February 1998.

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