Chromatin is a formidable barrier to transcription. Nucleosome density is lowest over the regulatory regions of active genes, and many repressed genes have a tightly positioned nucleosome over their core promoter. However, it has not been shown that nucleosome positioning is sufficient for repression or whether disrupting a core promoter nucleosome specifically can activate gene expression in the absence of activating signals. Here we show that disrupting the nucleosome over the core promoter of RNR3 is sufficient to drive preinitiation complex assembly and activate transcription in the absence of activating signals. Remodeling of chromatin over the RNR3 promoter requires the recruitment of the SWI/SNF complex by the general transcription factor TFIID. We found that disrupting the nucleosome over the RNR3 core promoter relieves its dependence on TFIID and SWI/SNF, indicating a functional link between these two complexes. These results suggest that the specific function of TAF(II)s is to direct the chromatin remodeling step through SWI/SNF recruitment, and not core promoter selectivity. Our results indicate that nucleosome placement plays a dominant role in repression and that the ability of the core promoter to position a nucleosome is a major determinant in TAF(II) dependency of genes in vivo.