Figure 5.

Point mutation of MyoD-CArG element abolishes MyoD PRR-DRR construct activity. C2.7 cells were stably transfected with 17.11wt and 17.11mut constructs containing either wild-type CArG or mutated CArG as shown in Figure 1. 4A: Cells were exposed to 50 nM or 100 nM trichostatin A for the indicated time before harvesting for β-galactosidase activity measurement as described in MATERIALS AND METHODS. 4B: DRR enhancer activity was measured in growing myoblasts stably transfected with the wild-type, mutated or consensus CArG-containing DRR reporter. Shown in both A and B are β-gal activity measurements from two series of experiments carried out with a whole population of stably transfected C2.7 cells. Control represents basal β-galactosidase activity in extracts from nontransfected C2.7.