Distinct functions for signal transducer and activator of transcription 1 and PU.1 in transcriptional activation of Fc γ receptor I promoter

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Abstract
The myeloid cell–specific expression and interferon-γ (IFN-γ) induction of Fc γ receptor I (FcγRI) requires cooperation between PU.1 and signal transducer and activator of transcription 1 (Stat1) by means of mechanisms that are unknown. We found that PU.1 and Stat1 mediated distinct functions in the activation of FcγRI promoter. The basal activity of the natural FcγRI promoter was strictly dependent on PU.1, and IFN-γ induction required both PU.1 and Stat1. Recruitment of TATA-binding protein (TBP) to the FcγRI promoter did not replace PU.1 in promoter activation, suggesting that TBP is not sufficient for FcγRI activation and that PU.1 mediates additional contacts with basal transcription machinery. In contrast, Stat1 did not interact with basal transcription machinery, but the Stat1-mediated activation of FcγRI promoter critically required CREB-binding protein (CBP)/p300. These results define functional cooperativity between PU.1 and Stat1 in FcγRI promoter activation, in which PU.1 appears to serve as a bridging factor with the basal transcription machinery and IFN-γ–mediated induction of transcription occurs through recruitment of CBP/p300 by Stat1.

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