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Titolo:
A NOVEL MYOGENIC REGULATORY CIRCUIT CONTROLS SLOW CARDIAC TROPONIN-C GENE-TRANSCRIPTION IN SKELETAL-MUSCLE/
Autore:
PARMACEK MS; IP HI; JUNG F; SHEN TL; MARTIN JF; VORA AJ; OLSON EN; LEIDEN JM;
Indirizzi:
UNIV CHICAGO,DEPT MED,MC 6088,ROOM G611,5841 S MARYLAND AVE CHICAGO IL 60637 UNIV CHICAGO,DEPT PATHOL CHICAGO IL 60637 UNIV MICHIGAN,DEPT INTERNAL MED ANN ARBOR MI 48109 MD ANDERSON CANC CTR,DEPT BIOCHEM & MOLEC BIOL HOUSTON TX 77030
Titolo Testata:
Molecular and cellular biology
fascicolo: 3, volume: 14, anno: 1994,
pagine: 1870 - 1885
SICI:
0270-7306(1994)14:3<1870:ANMRCC>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
CREATINE-KINASE GENE; ENHANCER-BINDING-FACTOR; ALPHA-ACTIN PROMOTER; LOOP-HELIX PROTEINS; LIGHT CHAIN-2 GENE; NUCLEAR PROTEINS; DNA-BINDING; ACCURATE TRANSCRIPTION; STRUCTURAL-ANALYSIS; UPSTREAM ELEMENTS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
87
Recensione:
Indirizzi per estratti:
Citazione:
M.S. Parmacek et al., "A NOVEL MYOGENIC REGULATORY CIRCUIT CONTROLS SLOW CARDIAC TROPONIN-C GENE-TRANSCRIPTION IN SKELETAL-MUSCLE/", Molecular and cellular biology, 14(3), 1994, pp. 1870-1885

Abstract

The slow/cardiac troponin C (cTnC) gene is expressed in three distinct striated muscle lineages: cardiac myocytes, embryonic fast skeletal myotubes, and adult slow skeletal myocytes. We have reported previously that cTnC gene expression in cardiac muscle is regulated by a cardiac-specific promoter/enhancer located in the 5' flanking region of the gene (bp -124 to +1). In this report, we demonstrate that the cTnC gene contains a second distinct and independent transcriptional enhancer which is located in the first intron. This second enhancer is skeletalmyotube specific and is developmentally up-regulated during the differentiation of myoblasts to myotubes. This enhancer contains three functionally important nuclear protein binding sites: a CACCC box, a MEF-2binding site, and a previously undescribed nuclear protein binding site, designated MEF-3, which is also present in a large number of skeletal muscle-specific transcriptional enhancers. Unlike most skeletal muscle-specific transcriptional regulatory elements, the cTnC enhancer does not contain a consensus binding site (CANNTG) for the basic helix-loop-helix (bHLH) family of transcription factors and does not directly bind MyoD-E12 protein complexes. Despite these findings, the cTnC enhancer can be transactivated by overexpression of the myogenic bHLH proteins, MyoD and myogenin, in C3H10T1/2 (10T1/2) cells. Electrophoretic mobility shift assays demonstrated changes in the patterns of MEF-2,CACCC, and MEF-3 DNA binding activities following the conversion of 10T1/2 cells into myoblasts and myotubes by stable transfection with a MyoD expression vector. In particular, MEF-2 binding activity was up-regulated in 10T1/2 cells stably transfected with a MyoD expression vector only after these cells fused and differentiated into skeletal myotubes. Taken together, these results demonstrated that distinct lineage-specific transcriptional regulatory elements control the expression of a single myofibrillar protein gene in fast skeletal and cardiac muscle. In addition, they show that bHLH transcription factors can indirectly transactivate the expression of some muscle-specific genes.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 09:34:08