Effect of fibrillation on acetylcholinesterase mRNA in cultured embryonic rat myotubes

Younkin, L.H.; McTiernan, Charles F.; Younkin, Samuel G.

doi:10.1016/0014-4827(88)90161-9

Cited by 3 publications

(5 citation statements)

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“…We observed an increase in the enzyme activity of AChE and its transcripts following electrical stimulation of cultured myotubes and a decrease following paralysis; our observations are consistent with previous reports in cultured rat muscle (Fluck and Strohman 1973;Koenig and Vigny 1978;Rieger et al 1980;Rubin et al 1980;Brockman et al 1982;Brockman et al 1984;Rubin 1985;Younkin et al 1988). Using a luciferase reporter assay, we demonstrated that the increase in endogenous AChE activity was accompanied by an increase in luciferase reporter activity in muscle cultures transfected with several Ache promoter fragments, consistent with an activation of transcript synthesis.…”

Section: Electrical Stimulation Increases Ache Expression By Increasisupporting

confidence: 92%

“…The modulation of AChE activity by contraction may be due in part to transcriptional mechanisms. Xenopus oocytes injected with poly(A) + RNA extracted from spontaneously contracting rat myotube cultures, expressed higher levels of translationally active AChE mRNA than did those injected with poly(A) + RNA from TTX-treated non-contracting cultures (Younkin et al 1988). In avian muscle, blockade of spontaneous contractions by application of TTX to isolated segments of cultured quail myotubes slightly increased the levels of AChE transcripts, suggesting that contraction-mediated changes in AChE transcription may differ in avian and mammalian muscle (Rossi et al 2000).…”

mentioning

confidence: 95%

“…Inhibition of spontaneous contractions by treatment with the Na 2+ channel blocker tetrodotoxin (TTX) reversibly prevents the increase in AChE activity in cultured rat myotubes (Brockman et al . 1984; Rubin 1985; Younkin et al . 1988).…”

mentioning

confidence: 99%

mentioning

confidence: 99%

“…Evidence suggests that at least two physiological parameters, membrane depolarization and mechanical stretch, mediate this response. Inhibition of spontaneous contractions by treatment with the Na 2+ channel blocker tetrodotoxin (TTX) reversibly prevents the increase in AChE activity in cultured rat myotubes (Brockman et al 1984;Rubin 1985;Younkin et al 1988). Alternatively, passive mechanical stretch of myotubes, without depolarizing the plasma membrane, leads to both an increase in AChE transcript levels and enzyme activity (Hubatsch and Jasmin 1997).…”

mentioning

confidence: 99%

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The regulation of acetylcholinesterase by cis‐elements within intron I in cultured contracting myotubes

Cohen

Randall

2006

Journal of Neurochemistry

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The onset of spontaneous contraction in rat primary muscle cultures coincides with an increase in acetylcholinesterase (AChE) activity. In order to establish whether contractile activity modulates the rate of AChE transcript synthesis, and what elements of the gene are determinant, we examined the promoter and intron I in contracting muscle cultures. Ache genomic fragments attached to a luciferase reporter were transfected into muscle cultures that were either electrically stimulated or paralyzed with tetrodotoxin to enhance or inhibit contractions, respectively. Cultures transfected with intron I-containing constructs showed a 2-fold increase in luciferase activity following electrical stimulation, compared to tetrodotoxin treatment, suggesting that this region contains elements responding to contractile activity. Deleting a 780 bp distal region within intron I, containing an N-box element at +890 bp, or introducing a 2-bp mutation within its core sequence, eliminated the contraction-induced response. In contrast, mutating an N-box element at +822 bp had no effect on the response. Furthermore, co-transfecting a dominant negative GA-binding protein (GABP), a transcription factor known to selectively bind N-box elements, reduced the stimulation-mediated increase. Our results suggest that the N-box within intron I at +890 bp is a regulatory element important in the transcriptional response of Ache to contractile activity in muscle.

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