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. Author manuscript; available in PMC: 2013 May 2.
Published in final edited form as: Mol Cell. 2010 Apr 9;38(1):41–53. doi: 10.1016/j.molcel.2010.01.042

Figure 4.

Figure 4

Retinoid acid receptor (RAR/RXR)-induced chromatin transitions allow NF1 to facilitate ligand-dependent transcription at the PEPCK promoter in vitro.

(A) Mononucleosomes derived from microccocal nuclease digestion of chromatinized template p(PEPCK-500)G assembled with hyperacetylated histone octamers using the RSF/NAP-1 system in vitro. (B) Nucleosomal mapping of the PEPCK promoter region within chromatinized p(PEPCK-500)G template assembled with hyperacetylated histone octamers (a-e) or hypoacetylated histone octamers (f, g) as a function of the presence of the factors indicated at the top of each panel. (C) The reaction scheme of the reconstituted transcription assays for (D) and (E). (D)In vitro reconstituted ligand-dependent transcription assays using the different chromatin templates indicated. (E) Optimal transcription from 30-nm chromatin fiber by RNAPII requires acetylation of core histones. (F) The reaction scheme of the reconstituted transcription assay for (G). (G) NF1 stimulates ligand-dependent transcription by RNAPII from compacted 30-nm chromatin fiber in the absence and presence of 0.1% Sarkosyl.