Androgen receptor (AR), a member of the nuclear receptor superfamily, is a modular protein comprised of a N-terminal domain (NTD), a central DNA binding domain (DBD) and a C-terminal ligand-binding domain (LBD). Previous structural and functional studies have shown that deletion of the LBD generates an AR molecule with full transcriptional activity in many transient transfection assays. In this study we show that deletion of either the NTD_1–478 (ARN) or LBD_680–919 (ARC) cripples AR transcriptional activity in chromatin. Both ARN and ARC mutants are impaired in binding to target genes in chromatin. Overexpression of SRC-1 coactivator partially rescued transcriptional and chromatin-binding defects of ARN and ARC mutants. Expression of SRC-1 also enhances the binding of the wild-type AR to chromatin, thus revealing a role of SRC-1 in promoting binding of AR to chromatin. We also demonstrate that expression of the AR NTD_1–501 in trans can substantially rescue the chromatin binding, but not the transcriptional defect of ARN, indicating that binding of AR to chromatin is a step separable from AR induced transcriptional activation. Finally we present evidence that, in contrast to transient transfection, AR NTD alone cannot efficiently activate transcription in chromatin.