HIV-1 Tat binds TAFII250 and represses TAFII250-dependent transcription of major histocompatibility class I genes

AUTOR(ES)

Weissman, Jocelyn D.

FONTE

National Academy of Sciences

RESUMO

HIV Tat, a transactivator of viral transcription, represses transcription of major histocompatibility (MHC) class I genes. Repression depends exclusively on the C-terminal domain of Tat, although the mechanism of this repression has not been known. We now show that repression results from the interaction of Tat with the TAFII250 component of the general transcription factor, TFIID. The C-terminal domain of Tat binds to a site on TAFII250 that overlaps the histone acetyl transferase domain, inhibiting TAFII250 histone acetyl transferase activity. Furthermore, promoters repressed by Tat, including the MHC class I promoter, are dependent on TAFII250 whereas those that are not repressed by Tat, such as SV40 and MuLV promoters, are independent of functional TAFII250. Thus, Tat repression of MHC class I transcription would be one mechanism by which HIV avoids immune surveillance.

Documentos Relacionados

• TAFII250-dependent transcription of cyclin A is directed by ATF activator proteins
• TAFII55 binding to TAFII250 inhibits its acetyltransferase activity
• Different functional domains of TAFII250 modulate expression of distinct subsets of mammalian genes
• Requirement for TAFII250 Acetyltransferase Activity in Cell Cycle Progression
• Requirement for TAFII250 Acetyltransferase Activity in Cell Cycle Progression