PMID- 11889044
OWN - NLM
STAT- MEDLINE
DCOM- 20020429
LR  - 20181113
IS  - 0261-4189 (Print)
IS  - 1460-2075 (Electronic)
IS  - 0261-4189 (Linking)
VI  - 21
IP  - 6
DP  - 2002 Mar 15
TI  - In vivo repression of an erythroid-specific gene by distinct corepressor 
      complexes.
PG  - 1389-97
AB  - To assess the mechanisms of repression of the erythroid-specific carbonic 
      anhydrase II (CAII) locus we used chromatin immunoprecipitation and show that an 
      NCoR-histone deacetylase (HDAC)3 complex is recruited by the nuclear receptor 
      v-ErbA to the intronic HS2 enhancer turning it into a potent silencer. 
      Furthermore we demonstrate that efficient CAII silencing requires binding of a 
      MeCP2-targeted HDAC-containing corepressor complex to the hypermethylated 
      CpG-island at the promoter. Activation of transcription by either AZAdC or 
      thyroid hormone results in loss of one of the two corepressor complexes. Thyroid 
      hormone further replaces the enhancer-bound NCoR-corepressor complex by the 
      TRAP220 coactivator. Treatment with the HDAC inhibitor trichostatin A (TSA) 
      causes activation of CAII transcription and histone H3 and H4 hyperacetylation at 
      the enhancer, apparently without affecting binding of the two corepressor 
      complexes. Unexpectedly, histone H3 and H4 at the fully repressed promoter are 
      already hyperacetylated despite the close apposition of the MeCP2-targeted HDAC 
      complex. Acetylation of histone H4, but not H3, at the promoter is moderately 
      increased following TSA treatment. Our data suggest that the hyperacetylated but 
      repressed CAII promoter is (partially) remodeled and primed for activation in 
      v-ErbA-transformed cells.
FAU - Rietveld, Luc E G
AU  - Rietveld LE
AD  - Department of Molecular Biology, NCMLS 191, University of Nijmegen, PO Box 9101, 
      6500 HB Nijmegen, The Netherlands.
FAU - Caldenhoven, Eric
AU  - Caldenhoven E
FAU - Stunnenberg, Hendrik G
AU  - Stunnenberg HG
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - EMBO J
JT  - The EMBO journal
JID - 8208664
RN  - 0 (Chromosomal Proteins, Non-Histone)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (MECP2 protein, human)
RN  - 0 (Methyl-CpG-Binding Protein 2)
RN  - 0 (NCOR1 protein, human)
RN  - 0 (Nuclear Proteins)
RN  - 0 (Nuclear Receptor Co-Repressor 1)
RN  - 0 (Oncogene Proteins v-erbA)
RN  - 0 (Repressor Proteins)
RN  - 06LU7C9H1V (Triiodothyronine)
RN  - EC 3.5.1.98 (Histone Deacetylases)
RN  - EC 3.5.1.98 (histone deacetylase 3)
RN  - EC 4.2.1.- (Carbonic Anhydrase II)
SB  - IM
MH  - Acetylation
MH  - Carbonic Anhydrase II/*genetics
MH  - Cell Line, Transformed
MH  - *Chromosomal Proteins, Non-Histone
MH  - *CpG Islands
MH  - DNA-Binding Proteins/*metabolism
MH  - *Gene Expression Regulation, Enzymologic
MH  - Histone Deacetylases/*metabolism
MH  - Humans
MH  - Methyl-CpG-Binding Protein 2
MH  - Nuclear Proteins/*metabolism
MH  - Nuclear Receptor Co-Repressor 1
MH  - Oncogene Proteins v-erbA/genetics/metabolism
MH  - Promoter Regions, Genetic
MH  - Protein Binding
MH  - Repressor Proteins/*metabolism
MH  - *Transcriptional Activation
MH  - Triiodothyronine/pharmacology
PMC - PMC125357
EDAT- 2002/03/13 10:00
MHDA- 2002/05/01 10:01
PMCR- 2003/03/15
CRDT- 2002/03/13 10:00
PHST- 2002/03/13 10:00 [pubmed]
PHST- 2002/05/01 10:01 [medline]
PHST- 2002/03/13 10:00 [entrez]
PHST- 2003/03/15 00:00 [pmc-release]
AID - cdf136 [pii]
AID - 10.1093/emboj/21.6.1389 [doi]
PST - ppublish
SO  - EMBO J. 2002 Mar 15;21(6):1389-97. doi: 10.1093/emboj/21.6.1389.