PMID- 19726504
OWN - NLM
STAT- MEDLINE
DCOM- 20091211
LR  - 20211020
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Print)
IS  - 0022-538X (Linking)
VI  - 83
IP  - 22
DP  - 2009 Nov
TI  - Loss of the Brm-type SWI/SNF chromatin remodeling complex is a strong barrier to 
      the Tat-independent transcriptional elongation of human immunodeficiency virus 
      type 1 transcripts.
PG  - 11569-80
LID - 10.1128/JVI.00742-09 [doi]
AB  - To elucidate the epigenetic regulation of Tat-independent human immunodeficiency 
      virus (HIV) transcription following proviral integration, we constructed an HIV 
      type 1 (HIV-1)-based replication-defective viral vector that expresses a reporter 
      green fluorescent protein (GFP) product from its intact long terminal repeat 
      (LTR). We transduced this construct into human tumor cell lines that were either 
      deficient in or competent for the Brm-type SWI/SNF complex. One day after 
      transduction, single cells that expressed GFP were sorted, and the GFP expression 
      profiles originating from each of these clones were analyzed. Unlike clones of 
      the SWI/SNF-competent cell line, which exhibited clear unimodal expression 
      patterns in all cases, many clones originating from Brm-deficient cell lines 
      either showed a broad-range distribution of GFP expression or were fully 
      silenced. The resorting of GFP-negative populations of these isolated clones 
      showed that GFP silencing is either reversible or irreversible depending upon the 
      proviral integration sites. We further observed that even in these silenced 
      clones, proviral gene transcription initiates to accumulate short transcripts of 
      around 60 bases in length, but no elongation occurs. We found that this 
      termination is caused by tightly closed nucleosome-1 (nuc-1) at the 5' LTR. Also, 
      nuc-1 is remodeled by exogenous Brm in some integrants. From these results, we 
      propose that Brm is required for the occasional transcriptional elongation of the 
      HIV-1 provirus in the absence of Tat. Since the Brm-type SWI/SNF complex is 
      expressed at marginal levels in resting CD4+ T cells and is drastically induced 
      upon CD4+ T-cell activation, we speculate that it plays crucial roles in the 
      early Tat-independent phase of HIV transcription in affected patients.
FAU - Mizutani, Taketoshi
AU  - Mizutani T
AD  - Division of Host-Parasite Interaction, Department of Microbiology and Immunology, 
      Institute of Medical Science, University of Tokyo, Tokyo, Japan.
FAU - Ishizaka, Aya
AU  - Ishizaka A
FAU - Tomizawa, Mariko
AU  - Tomizawa M
FAU - Okazaki, Takuya
AU  - Okazaki T
FAU - Yamamichi, Nobutake
AU  - Yamamichi N
FAU - Kawana-Tachikawa, Ai
AU  - Kawana-Tachikawa A
FAU - Iwamoto, Aikichi
AU  - Iwamoto A
FAU - Iba, Hideo
AU  - Iba H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090902
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (RNA, Viral)
RN  - 0 (SMARCA2 protein, human)
RN  - 0 (Transcription Factors)
RN  - 0 (Transcriptional Elongation Factors)
RN  - 0 (tat Gene Products, Human Immunodeficiency Virus)
SB  - IM
MH  - Cell Line, Tumor
MH  - Chromatin Assembly and Disassembly/*genetics
MH  - Genetic Vectors/genetics
MH  - HIV-1/*genetics/physiology
MH  - Humans
MH  - RNA, Viral/biosynthesis
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Transcription Factors/genetics/physiology
MH  - Transcription, Genetic/genetics
MH  - Transcriptional Elongation Factors/*genetics/physiology
MH  - Transduction, Genetic
MH  - Virus Replication/genetics
MH  - tat Gene Products, Human Immunodeficiency Virus/*genetics/physiology
PMC - PMC2772682
EDAT- 2009/09/04 06:00
MHDA- 2009/12/16 06:00
PMCR- 2010/05/01
CRDT- 2009/09/04 06:00
PHST- 2009/09/04 06:00 [entrez]
PHST- 2009/09/04 06:00 [pubmed]
PHST- 2009/12/16 06:00 [medline]
PHST- 2010/05/01 00:00 [pmc-release]
AID - JVI.00742-09 [pii]
AID - 0742-09 [pii]
AID - 10.1128/JVI.00742-09 [doi]
PST - ppublish
SO  - J Virol. 2009 Nov;83(22):11569-80. doi: 10.1128/JVI.00742-09. Epub 2009 Sep 2.