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Sci. STKE, 26 April 2005
Vol. 2005, Issue 281, p. tw161
[DOI: 10.1126/stke.2812005tw161]

EDITORS' CHOICE

CELL CYCLE Activating ATM with Broken DNA

Cells depend on a checkpoint mechanism that stops cell division when damaged DNA is detected, but which molecular sensors "see" breaks in DNA strands is unclear. DNA damage leads to activation of the protein kinase ATM, the product of the gene mutated in ataxia-telangiectasia (a human disease characterized by sensitivity to radiation and predisposition to cancer). Lee and Paull (see the Perspective by Abraham and Tibbetts) describe an in vitro assay in which dimeric ATM (but not the monomeric enzyme) is activated by broken DNA molecules in the presence of the MRN complex, a complex of three other proteins. The MRN complex interacts with DNA and recruits ATM to the DNA-bound complex. Thus, adenosine triphosphate-dependent DNA unwinding by the MRN complex appears to be a necessary step in the activation of ATM.

J.-H. Lee, T. T. Paull, ATM activation by DNA double-strand breaks through the Mre11-Rad50-Nbs1 complex. Science 308, 551-554 (2005). [Abstract] [Full Text]

R. T. Abraham, R. S. Tibbetts, Guiding ATM to broken DNA. Science 308, 510-511 (2005). [Summary] [Full Text]

Citation: Activating ATM with Broken DNA. Sci. STKE 2005, tw161 (2005).

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