Structure, evolution, and regulation of a fast skeletal muscle troponin I gene.

Baldwin, Albert S.; Kittler, Ellen L. W.; Emerson, Charles P.

doi:10.1073/pnas.82.23.8080

Cited by 86 publications

(52 citation statements)

References 39 publications

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“…TnILacZ1 contains 530 bp of 5Ј-flanking DNA, exon 1, intron 1, and the first (untranslated) part of exon 2 of the quail TnIfast gene (Baldwin et al, 1985), linked to a 5.2-kb SmaI/ EcoRI fragment of pRSVZ (MacGregor et al, 1987) containing promoterless E. coli LacZ sequences and SV40 splicing and polyadenylation sequences (see construct maps in Fig. 1).…”

Section: Experimental Procedures Dna Constructsmentioning

confidence: 99%

TnIfast IRE enhancer: Multistep developmental regulation during skeletal muscle fiber type differentiation

Hallauer

Hastings

2002

Developmental Dynamics

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To identify developmental steps leading to adult skeletal muscle fiber-type-specific gene expression, we carried out transgenic mouse studies of the IRE enhancer of the quail TnIfast gene. Histochemical analysis of IRE/herpesvirus tk promoter/␤-galactosidase reporter transgene expression in adult muscle directly demonstrated IRE-driven fast vs. slow fiber-type specificity, and IIB>IIX>IIA differential expression among the fast fiber types: patterns similar to those of native-promoter TnIfast constructs. These tissue-and cell-type specificities are autonomous to the IRE and do not depend on interactions with a muscle gene promoter. Developmental studies showed that the adult pattern of IRE-driven transgene expression emerges in three steps: (1) activation during the formation of primary embryonic (presumptive slow) muscle fibers; (2) activation, to markedly higher levels, during formation of secondary (presumptive fast) fibers, and (3) differential augmentation of expression during early postnatal maturation of the IIB, IIX, IIA fast fiber types. These results provide insight into the roles of gene activation and gene repression mechanisms in fiber-type specificity and can account for apparently disparate results obtained in previous studies of TnI isoform expression in development. Each of the three IRE-driven developmental steps is spatiotemporally associated with a different major regulatory event at the fast myosin heavy chain gene cluster, suggesting that diverse muscle gene families respond to common, or tightly integrated, regulatory signals during multiple steps of muscle fiber differentiation.

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Section: Experimental Procedures Dna Constructsmentioning

confidence: 99%

TnIfast IRE enhancer: Multistep developmental regulation during skeletal muscle fiber type differentiation

Hallauer

Hastings

2002

Developmental Dynamics

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“…Each has a large first intron that interrupts the 5′ noncoding region or the first two codons of the gene. This structure is present in both Drosophila (Basi and Storti, 1986;Falkenthal et al, 1984;Geyer and Fyrberg, 1986;Marin et al, 2004;Mas et al, 2004;Parker et al, 1985) and vertebrate muscle genes (Baldwin et al, 1985;Chang et al, 1985;Fornwald et al, 1982;Nabeshima et al, 1984;Strehler et al, 1986). Transcriptional enhancer elements are located in the first intron of a number of such muscle genes (Konieczny and Emerson, 1987;Marin et al, 2004;Mas et al, 2004;Meredith and Storti, 1993;Ng et al, 1989;Yutzey et al, 1989).…”

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confidence: 99%

Transcriptional regulation of the Drosophila melanogaster muscle myosin heavy-chain gene

Hess

Singer

Trinh

et al. 2007

Gene Expression Patterns

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We show that a 2.6 kb fragment of the muscle myosin heavy-chain gene (Mhc) of Drosophila melanogaster (containing 458 base pairs of upstream sequence, the first exon, the first intron and the beginning of the second exon) drives expression in all muscles. Comparison of the minimal promoter to Mhc genes of ten Drosophila species identified putative regulatory elements in the upstream region and in the first intron. The first intron is required for expression in four small cells of the tergal depressor of the trochanter (jump) muscle and in the indirect flight muscle. The 3′ end of this intron is important for Mhc transcription in embryonic body wall muscle and contains AT-rich elements that are protected from DNase I digestion by nuclear proteins of Drosophila embryos. Sequences responsible for expression in embryonic, adult body wall and adult head muscles are present both within and outside the intron. Elements important for expression in leg muscles and in the large cells of the jump muscle flank the intron. We conclude that multiple transcriptional regulatory elements are responsible for Mhc expression in specific sets of Drosophila muscles. KeywordsDrosophila melanogaster; muscle; myosin heavy chain; transcription; enhancer; gene regulation Drosophila melanogaster is unusual in having a single muscle myosin heavy-chain gene (Mhc) (Bernstein et al., 1983;Rozek and Davidson, 1983), rather than a Mhc multigene family (see Emerson and Bernstein, 1987 for review). Alternative splicing of the primary transcripts from this gene yields multiple isoforms of the protein (Collier et al., 1990;George et al., 1989;Hastings and Emerson, 1991;Kazzaz and Rozek, 1989;Kronert et al., 1991;Zhang and Bernstein, 2001). Drosophila Mhc is expressed in all muscles at embryonic, larval, pupal and adult stages. Thus several stage-or muscle-specific enhancer elements may regulate its transcription.Transcriptional regulatory regions for a number of Drosophila muscle genes have been mapped, resulting in the identification of both unique and shared cis-acting elements (Arredondo et al., 2001;Kelly et al., 2002;Marin et al., 2004;Mas et al., 2004;Meredith and Storti, 1993). The latter includes E-boxes that bind helix-loop-helix transcription factors and MEF2 sites that bind MEF2 protein (Bour et al., 1995; Lilly et al., 1995). E-boxes, MEF2 sites and their binding factors positively regulate vertebrate muscle gene expression as well (see Molkentin and Olson, 1996 for review).* Corresponding author. Tel.: +1-619-594-5629; fax: +1-619-594-5676; E-mail address: sbernst@sunstroke.sdsu.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal dis...

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“…In contrast with the avian fast skeletal-muscle TnI gene and the human slow skeletal-muscle TnI gene, the first exon of the cardiac TnI gene contains the start codon. The avian fast skeletal-muscle, rat and human slow skeletal-muscle TnI genes, like several other muscle-specific genes, have a first exon that is untranslated [12,13,27,28]. The intron-exon structure of the avian fast skeletal-muscle, the human slow skeletal-muscle and rat and mouse cardiac genes are completely conserved for exons 5, 6 and 7, which encode the majority of the protein sequence [13,29].…”

Section: Gene Structure and Putative Regulatory Motifsmentioning

confidence: 99%

Regulation of the rat cardiac troponin I gene by the transcription factor GATA-4

Murphy

Thompson

Peng

et al. 1997

Biochemical Journal

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Troponin I is a thin-filament contractile protein expressed in striated muscle. There are three known troponin I genes which are expressed in a muscle-fibre-type-specific manner in mature animals. Although the slow skeletal troponin I isoform is expressed in fetal and neonatal heart, the cardiac isoform is restricted in its expression to the myocardium at all developmental stages. To study the regulation of this cardiac-specific and developmentally regulated gene in vitro, the rat cardiac troponin I gene was cloned. Transient transfection assays were performed with troponin I–luciferase fusion plasmids to characterize the regulatory regions of the gene. Proximal regions of the upstream sequence were sufficient to support high levels of expression of the reporter gene in cardiocytes and relatively low levels in other cell types. The highest luciferase activity in the cardiocytes was noted with a plasmid that included the region spanning -896 to +45 of the troponin I genomic sequence. Co-transfection of GATA-4, a recently identified cardiac transcription factor, with troponin I–luciferase constructs permitted high levels of luciferase expression in non-cardiac cells. Electrophoretic mobility-shift assays demonstrated specific binding of GATA-4 to oligonucleotides representative of multiple sites of the troponin I sequence. Mutation of a proximal GATA-4 DNA-binding site decreased transcriptional activation in transfected cardiocytes. These results indicate that the proximal cardiac troponin I sequence is sufficient to support high levels of cardiac-specific gene expression and that the GATA-4 transcription factor regulates troponin I–luciferase expression in vitro.

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Structure, evolution, and regulation of a fast skeletal muscle troponin I gene.

Cited by 86 publications

References 39 publications

TnIfast IRE enhancer: Multistep developmental regulation during skeletal muscle fiber type differentiation

TnIfast IRE enhancer: Multistep developmental regulation during skeletal muscle fiber type differentiation

Transcriptional regulation of the Drosophila melanogaster muscle myosin heavy-chain gene

Regulation of the rat cardiac troponin I gene by the transcription factor GATA-4

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