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Requirement for SWI/SNF chromatin‐remodeling complex in Tat‐mediated activation of the HIV‐1 promoter
Author(s) -
Tréand Céline,
du Chéné Isaure,
Brès Vanessa,
Kiernan Rosemary,
Benarous Richard,
Benkirane Monsef,
Emiliani Stéphane
Publication year - 2006
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/sj.emboj.7601074
Subject(s) - chromatin remodeling , biology , transactivation , chromatin structure remodeling (rsc) complex , chromatin , hiv long terminal repeat , microbiology and biotechnology , long terminal repeat , swi/snf , smarca4 , acetylation , histone , chia pet , dna , transcription factor , genetics , gene , gene expression
Activation of the human immunodeficiency virus type‐1 (HIV‐1) promoter in infected cells requires the sequential recruitment of several cellular factors to facilitate the formation of a processive elongation complex. The nucleosomal reorganization of the HIV‐1 long terminal repeat (LTR) observed upon Tat stimulation suggests that chromatin‐remodeling complexes could play a role during this process. Here, we reported that Tat interacts directly with Brm, a DNA‐dependent ATPase subunit of the SWI/SNF chromatin‐remodeling complex, to activate the HIV‐1 LTR. Inhibition of Brm via small interfering RNAs impaired Tat‐mediated transactivation of an integrated HIV‐1 promoter. Furthermore, Brm is recruited in vivo to the HIV‐1 LTR in a Tat‐dependent manner. Interestingly, we found that Tat/Brm interaction is regulated by Tat lysine 50 acetylation. These data show the requirement of Tat‐mediated recruitment of SWI/SNF chromatin‐remodeling complex to HIV‐1 promoter in the activation of the LTR.