Research Paper Volume 1, Issue 1 pp 109—121

SIRT6 stabilizes DNA-dependent Protein Kinase at chromatin for DNA double-strand break repair

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Figure 5. Dynamic association of SIRT6 and DNA-PKcs with chromatin flanking site-specific DNA DSBs. (a) SIRT6 occupancy at chromatin flanking DSBs induced by I-PpoI. Quantitative real-time PCR amplification of DNA sequences flanking the I-PpoI site from ChIPs performed with SIRT6 antibodies. Data are normalized to no I-PpoI (control) samples. (b) DNA-PKcs occupancy at chromatin flanking DSBs induced by I-PpoI, determined as for SIRT6 in (a). (c) DNA-PKcs occupancy at the indicated distances from an I-SceI DSB site in SIRT6 KD and controls cells. Data are normalized to no I-SceI controls. (d) DNA-PKcs occupancy at chromatin adjacent to (+60 to +223 bp) an I-SceI DSB site, following retroviral over-expression of Flag-tagged wild-type SIRT6 (S6WT), catalytically inactive SIRT6 (S6HY), or empty vector control (pBabe). In all panels, SIRT6 KD cells were generated with S6KD2 shRNA, and the data represent the mean +/- S.E.