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Titolo:
A SERUM RESPONSE FACTOR-DEPENDENT TRANSCRIPTIONAL REGULATORY PROGRAM IDENTIFIES DISTINCT SMOOTH-MUSCLE CELL SUBLINEAGES
Autore:
KIM S; IP HS; LU MM; CLENDENIN C; PARMACEK MS;
Indirizzi:
UNIV CHICAGO,DEPT MED,MC 6088,5841 S MARYLAND AVE CHICAGO IL 60637 UNIV CHICAGO,DEPT MED CHICAGO IL 60637
Titolo Testata:
Molecular and cellular biology
fascicolo: 4, volume: 17, anno: 1997,
pagine: 2266 - 2278
SICI:
0270-7306(1997)17:4<2266:ASRFTR>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
ALPHA-ACTIN GENE; TROPONIN-C GENE; DNA-BINDING ACTIVITY; GROWTH-FACTOR; SKELETAL-MUSCLE; MYOGENIN GENE; MADS BOX; EXPRESSION; PROMOTER; PROTEINS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
68
Recensione:
Indirizzi per estratti:
Citazione:
S. Kim et al., "A SERUM RESPONSE FACTOR-DEPENDENT TRANSCRIPTIONAL REGULATORY PROGRAM IDENTIFIES DISTINCT SMOOTH-MUSCLE CELL SUBLINEAGES", Molecular and cellular biology, 17(4), 1997, pp. 2266-2278

Abstract

The SM22 alpha promoter has been used as a model system to define themolecular mechanisms that regulate smooth muscle cell (SMC) specific gene expression during mammalian development. The SM22 alpha gene is expressed exclusively in vascular and visceral SMCs during postnatal development and is transiently expressed in the heart and somites duringembryogenesis. Analysis of the SM22 alpha promoter in transgenic micerevealed that 280 bp of 5' flanking sequence is sufficient to restrict expression of the lacZ reporter gene to arterial SMCs and the myotomal component of the somites. DNase I footprint and electrophoretic mobility shift analyses revealed that the SM22 alpha promoter contains six nuclear protein binding sites (designated smooth muscle elements [SMEs]-1 to -6, respectively), two of which bind serum response factor (SRF) (SME-1 and SME-4). Mutational analyses demonstrated that a two-nucleotide substitution that selectively eliminates SRF binding to SME-3 decreases SM22 alpha promoter activity in arterial SMCs by approximately 90%. Moreover, mutations that abolish binding of SRF to SME-I and SME-4 or mutations that eliminate each SME-3 binding activity totally abolished SM22 alpha promoter activity in the arterial SMCs and somitesof transgenic mice. Finally, we have shown that a multimerized copy of SME-4 (bp -190 to -110) when linked to the minimal SM22 alpha promoter (bp -90 to +41) is necessary and sufficient to direct high-level transcription in an SMC lineage-restricted fashion. Taken together, these data demonstrate that distinct transcriptional regulatory programs control SM22 alpha gene expression in arterial versus visceral SMCs, Moreover, these data are consistent with a model in which combinatorial interactions between SRF and other transcription factors that bind to SME-4 (and that bind directly to SRF) activate transcription of the SM22 alpha gene in arterial SMCs.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/09/20 alle ore 13:39:00