In vivo and in vitro analysis of electricalactivity-dependent expression of muscle acetylcholine receptor genes usingadenovirus.

Bessereau, Jean-Louis; Stratford-Perricaudet, Leslie D.; Piette, Jacques; Poupon, Chantal Le; Changeux, J P

doi:10.1073/pnas.91.4.1304

Cited by 72 publications

(59 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous work has suggested a role for E boxes in depolarization transcription coupling. Our observations on the chick AChR =-subunit enhancer confirm and extend the findings of lkssereau et al, [19] who recently showed that, in transgenic animals, constructs carrying lacZ under the control of an 850-bp =-subunit promoter are stimulated by denervation only when the 3' E box in the =-subunit enhancer is intact. Tang et ai, [20] were able to eliminate the response to denervation in a transgene composed of the human growth hormone coding region and a mouse AChR ~;-subunit regulatory region in which the single E box had been mutated.…”

Section: Discussionsupporting

confidence: 80%

See 1 more Smart Citation

The depolarization response element in acetylcholine receptor genes is a dual‐function E box

Huang

Schmidt

1995

FEBS Letters

View full text Add to dashboard Cite

All acetylcholine receptor subunit genes contain E boxes and are blocked by membrane depolarization. We have used transfected C2C12 myogenic cells to investigate the response, to electrical stimulation and KCi, of wildtype and mutant regulatory regions of the chick acetylcboline receptor a, 7 and B subunit, and the mouse MLC genes. Poh,t mutations revealed that E boxes function as activating elements targeted by the depolarization signal. These experiments suggest, and Insertion of u depolarization response element into an unrelated promoter confirms, that plasma membrane depolarization switches the depolarization response element from an activating to a repressive mode.

show abstract

Section: Discussionsupporting

confidence: 80%

“…Recently Bessereau et al [19] and Tang et al [20] reported that E box mutation abolishes the denervation response of reporter constructs driven by the chick 0t and the mouse 8 promoter, respectively. Since it is believed that the activation * Corresponding author.…”

Section: Introductionmentioning

confidence: 99%

The depolarization response element in acetylcholine receptor genes is a dual‐function E box

Huang

Schmidt

1995

FEBS Letters

View full text Add to dashboard Cite

show abstract

“…Because of reports that all or many of these myogenic factors can bind (26) and transactivate nAChR (21)(22)(23)(24)(25) and MuSK (11,17) promoters, one may propose that they do not compensate for myogenin but may act independently to regulate nAChR and MuSK gene expression. We do not think this is the case based on the following knock-out studies.…”

Section: Discussionmentioning

confidence: 99%

“…Inspection of the three different E-boxes indicates that E-box 1 harbors a sequence (CAGCTG) that is very similar to those found in nAChR promoters that are transactivated by myogenin and mediate muscle-specific and activity-dependent gene expression (21)(22)(23)(24)(25). In contrast, E-box 2 (CACTTG) and E-box 3 (CATCTG) are less similar.…”

Section: A Conserved 200-bp 5ј-flanking Musk Promotermentioning

confidence: 99%

“…Vivo-Previous studies of nAChR promoter regulation identified critical E-boxes, which are most proximal to the transcription initiation sites, as important mediators of bHLH binding and gene activation (21)(22)(23)(24)(25). Chromatin immunoprecipitation assays have suggested that all four bHLH MyoD family members can bind and activate nAChR promoters, suggesting a redundant function for these proteins in regulating nAChR gene expression (26).…”

Section: Myogenin Is Essential For Differentiation-and Activity-depenmentioning

confidence: 99%

See 1 more Smart Citation

Characterization of a Muscle-specific Enhancer in Human MuSK Promoter Reveals the Essential Role of Myogenin in Controlling Activity-dependent Gene Regulation

Tang

Veldman

Goldman

2006

Journal of Biological Chemistry

View full text Add to dashboard Cite

Neuromuscular synaptogenesis is initiated by the release of agrin from motor neurons and the activation of the receptor tyrosine kinase, MuSK, in the postsynaptic membrane. MuSK gene expression is regulated by nerve-derived agrin and muscle activity. Agrin stimulates synapse-specific MuSK gene expression by activating GABP ␣␤ transcription factors in endplate-associated myonuclei. In contrast, the mechanism by which muscle activity regulates MuSK gene expression is not known. We report on a 60-bp MuSK enhancer that confers promoter regulation by muscle differentiation, changes in intracellular calcium, and muscle activity. Within this enhancer, we identified a single E-box that is essential for this regulation. This E-box binds myogenin, and we showed that myogenin is necessary for not only MuSK but also nAChR gene regulation by muscle activity. Surprisingly, the same E-box functions in vivo to mediate muscle-specific and differentiation-dependent gene induction in zebrafish, suggesting an evolutionary conserved mechanism of regulation of synaptic protein gene expression.

show abstract

Regulation and functional significance of utrophin expression at the mammalian neuromuscular synapse

Gramolini

Jasmin

2000

Microsc. Res. Tech.

View full text Add to dashboard Cite

Duchenne muscular dystrophy (DMD) is caused by the absence of full‐length dystrophin molecules in skeletal muscle fibers. In normal muscle, dystrophin is found along the length of the sarcolemma where it links the intracellular actin cytoskeleton to the extracellular matrix, via the dystrophin‐associated protein (DAP) complex. Several years ago, an autosomal homologue to dystrophin, termed utrophin, was identified and shown to be expressed in a variety of tissues, including skeletal muscle. However, in contrast to the localization of dystrophin in extrajunctional regions of muscle fibers, utrophin preferentially accumulates at the postsynaptic membrane of the neuromuscular junction in both normal and DMD adult muscle fibers. Since it has recently been suggested that the upregulation of utrophin might functionally compensate for the lack of dystrophin in DMD, considerable interest is now directed toward the elucidation of the various regulatory mechanisms presiding over expression of utrophin in normal and dystrophic skeletal muscle fibers. In this review, we discuss some of the most recent data relevant to our understanding of the impact of myogenic differentiation and innervation on the expression and localization of utrophin in skeletal muscle fibers. Microsc. Res. Tech. 49:90–100, 2000. © 2000 Wiley‐Liss, Inc.

show abstract

In vivo and in vitro analysis of electricalactivity-dependent expression of muscle acetylcholine receptor genes usingadenovirus.

Cited by 72 publications

References 42 publications

The depolarization response element in acetylcholine receptor genes is a dual‐function E box

The depolarization response element in acetylcholine receptor genes is a dual‐function E box

Characterization of a Muscle-specific Enhancer in Human MuSK Promoter Reveals the Essential Role of Myogenin in Controlling Activity-dependent Gene Regulation

Regulation and functional significance of utrophin expression at the mammalian neuromuscular synapse

Contact Info

Product

Resources

About