1: Nat Cell Biol. 2002 Feb;4(2):140-7. 

IFN-Stimulated transcription through a TBP-free acetyltransferase complex
escapes viral shutoff.

Paulson M, Press C, Smith E, Tanese N, Levy DE.

Department of Pathology, Kaplan Comprehensive Cancer Center, New York University
School of Medicine, 550 First Avenue, New York, New York 10016, USA.

Type I interferon (IFN) stimulates transcription through a heteromeric
transcription factor that contains tyrosine-phosphorylated STAT2. We show that
STAT2 recruits histone acetyltransferases (HAT) through its transactivation
domain, resulting in localized transient acetylation of histones. GCN5, but not
p300/CBP or PCAF, is required for STAT2 function. However, GCN5 function is
impaired by the transcriptional antagonist, adenovirus E1A oncoprotein. The
TFIID component TAF(II)130 potentiates STAT2 function, but TAF(II)28 or the HAT
activity of TAF(II)250 do not, and transcriptional induction can proceed
independently of the TATA-binding protein, TBP. Moreover, IFN-stimulated
transcription was resistant to poliovirus-targeted degradation by TBP, and
continued despite host-cell transcriptional shutoff during poliovirus infection.
We conclude that a non-classical transcriptional mechanism combats an
anticellular action of poliovirus, through a TBP-free TAF-containing complex and
GCN5.

PMID: 11802163 [PubMed - indexed for MEDLINE]


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