Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Subscribe

Sci. Signal., 14 September 2010
Vol. 3, Issue 139, p. ec284
[DOI: 10.1126/scisignal.3139ec284]

EDITORS' CHOICE

DNA Repair UnSIRT6ain Repair

Guy Riddihough

Science, AAAS, Washington, DC 20005, USA

Efficient and accurate repair of double-strand DNA breaks is critical for genome stability and involves a process known as homologous recombination. During repair of the sheared ends, the DNA must be resected by trimming one of the two strands on either side of the break. For the repair to be accurate, the remaining single-stranded DNA (ssDNA) has to be bound by the ssDNA-binding protein, RPA, after which the ssDNA can then bind homologous sequences. Kaidi et al. found that the mammalian deacetylase, SIRT6 (which has been implicated in maintaining genome stability), was critical for resection. At sites of DNA damage, SIRT6 deacetylated and activated CtIP (a protein important for resection), ensuring that resection occurred at the appropriate place and time.

A. Kaidi, B. T. Weinert, C. Choudhary, S. P. Jackson, Human SIRT6 promotes DNA end resection through CtIP deacetylation. Science 329, 1348–1353 (2010). [Abstract] [Full Text]

Citation: G. Riddihough, UnSIRT6ain Repair. Sci. Signal. 3, ec284 (2010).



To Advertise     Find Products


Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882