The multiprotein human SWI-SNF (hSWI-SNF) complex is a chromatin-remodeling
machine that facilitates transcription by overcoming chromatin-mediated ge
ne repression. We had previously shown that hSNF5/INl1, an intrinsic, consi
stent component of the hSWI/SNF complex, is associated with Epstein-Barr nu
clear antigen 2 (EBNA2) and have proposed that EBNA2 directs this complex t
o key EBNA2-responsive viral and cellular genes. Using chromatin immunoprec
ipitation and quantitative PCR, we show that antibodies directed against co
mponents of the hSWI-SNF complex preferentially precipitate chromatin-assoc
iated DNA that contains a targeted EBNA2-responsive element in the context
of both episomal and cellular chromatin. This enrichment does not occur in
EBNA2-negative cells or when the EBNA2-responsive element is mutated. The s
table association of the hSWI-SNF complex with the EBNA2-responsive promote
r can also be disrupted by deletion of the TATA element, suggesting that EB
NA2 in itself is insufficient to mediate stable targeting of the hSWI-SNF c
omplex. These results demonstrate that recruitment of the hSWI-SNF complex
to selected promoters can occur in vivo through its interaction with site-s
pecific activator proteins and that stable targeting may require the presen
ce of basal transcription factors.