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. Author manuscript; available in PMC: 2013 Dec 11.
Published in final edited form as: Science. 2011 Jun 17;332(6036):10.1126/science.1196766. doi: 10.1126/science.1196766

Fig. 3.

Fig. 3

Presence of SIN3-HDAC1 at Per1 promoter depends on PER and PSF. (A) ChIP assays from lung (CT 10) comparing PSF, SIN3A, and HDAC1 at the Per1 proximal E-box or control promoter in wild-type littermates (white) and Per1−/−; Per2−/− mice (black). (B) ChIP assays, as in (A), from mouse fibroblasts after introduction of point-mutant control PSF shRNA (white) or after depletion of PSF by effective PSF shRNA (black). (C) ChIP assays, as in (A), from lung (CT14) comparing acetylation of HDAC1 targets (at bottom) at the Per1 E-box site or control promoter in wild-type littermates (white) and Per1−/−; Per2−/− mice (black). (D) ChIP assays, as in (C), from fibroblasts after introduction of point-mutant control PSF shRNA (white) or after depletion of PSF by effective PSF shRNA (black). ChIP values are plotted relative to the signal at an arbitrary internal control genomic region (SOM methods). All show mean +/− SEM of triplicate experiments and are representative of 2-4 experiments.