Abstract
Both N-CoR and SMRT bind to unliganded nuclear receptors and repress transcription through recruitment of HDAC3. A central question in TR mediated transcriptional repression is the differential role of N-CoR and SMRT complexes. Here we show that both N-CoR and SMRT are independently involved in transcriptional repression of multiple TR-target genes including BCL3, Spot14, FAS and ADRB2. We show that either siRNA treatment against NCoR or SMRT is sufficient for the repression of multiple TR-target genes. Our data suggest that the SMRT and N-CoR are independently recruited to various TR target genes through the siRNA experiments. We also show that unliganded, corepressor-free TR is defective in repression and may interact with coactivator, P300. Furthermore, overexpression of N-CoR can restore repression of endogenous genes after knocking-down SMRT. Together, our data reveal the differential roles of corepressor complexes and provide evidence for the possible interaction between unliganded, corepressor-free TR and coactivators. ∗ This work was supported by the Korea Research Foundation Grant funded by the Korean Government(MOEHRD) (KRF-2006-331-E00036) and (KRF-2005-042-E00022).
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