Cells proceed with caution. If they detect damage to themselves, they pull over for repairs before going on to the next stage in their division cycle. Researchers have now discovered a link between two of the key players in this fail-safe mechanism.
Ultraviolet light, ionizing radiation and a variety of chemicals damage DNA, breaking either or both of its strands. When a cell senses this damage, either of two related molecules known as ATR and ATM, which perform many tasks in the cell’s damage-repair network, springs into action.
Working with human cell cultures, Xiao-Fan Wang and colleagues of the Duke University Medical Center, Durham, North Carolina, have found that one of the functions of ATM and ATR is to activate another protein called human Rad17 (Nature, Vol. 411, No. 6840, 21 Jun 2001). hRad17 then seems to load yet another set of proteins onto the damaged DNA strand to begin the repair process.
Malfunctions in DNA repair are involved in many cancers, and there is a rare and fatal genetic disorder involving mutations to the ATM gene — sufferers have immune deficiencies and a high rate of cancer. A better understanding of the checkpoints that prevent damaged cells from dividing could lead to better models, and eventually new therapies, for cancer.
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