Some exciting recent advances in understanding how the chromatin state can affect the response to DNA damage. With all the usual thoroughness and clever use of in vitro reconstituted systems, Dan Durocher's lab shows that 53BP1 recognizes and is recruited to dimethylated and ubiquitinated histones (marks present at the site of DNA damage). In a similar vein, Michael Yaffe's lab shows that the BET domain-containing protein Brd4 (isoform B, specifically) influences the number and size of DNA damage foci in the nucleus by modulating chromatin compaction. Less clear to me exactly what implications this may have in vivo, but a nice use of high-content RNAi screening and the small molecule Brd4 inhibitor JQ-1 to dissect the phenotype. I wonder if cancer cells, due to modifications in the chromatin state associated with mutation, etc, become more or less susceptible to specific forms of DNA damage?