P300 is involved in formation of the TBP-TFIIA-containing basal transcription complex, TAC.

Abstract

We have recently identified a novel basal transcription complex, TAC, that is present and active in embryonal carcinoma (EC) cells but not in other adult cells such as COS7. In the search for factors involved in TAC formation, we found that expression of the adenoviral 12S E1A oncoprotein abolishes TAC formation in EC cells. This effect of E1A depends on its N-terminal domain that is essential for cell differentiation and that targets the transcriptional coactivators p300 and PCAF. Expression of p300 lacking its major E1A interaction domain, CH3, restores TAC formation in the presence of E1A, in a bromodomain- and HAT domain-dependent manner. Consistently, the unprocessed TFIIAalphabeta precursor that is selectively assembled into TAC is acetylated preferentially compared with the processed subunits present in 'free' TFIIA. Intriguingly, expression of p300 in COS7 cells that do not contain detectable levels of TAC instigates formation of TAC from endogenous components. Our data suggest that p300 plays a role in formation of the TBP-TFIIA-containing basal transcription complex, TAC.