Control of acetylcholinesterase gene expression during myogenesis.
Acetylcholinesterase (AChE) and the nicotinic acetylcholine receptor show enhanced expression upon differentiation of C2-C12 myoblasts into myotubes. Northern blots and RNAase protection show substantial increases in the mRNAs encoding both proteins. In contrast to transcriptional control of gene expression of acetylcholine receptor subunits during differentiation, Ache mRNA levels increase through stabilization of the transcript. The transcriptional rate remains unchanged during Ache mRNA accumulation, whereas transcription rate increase for the receptor subunits. Inhibition of protein synthesis produces a dramatic superinduction of Ache mRNA in undifferentiated cells without affecting transcription rates, suggesting the presence of labile proteins that uniquely destabilize the mRNA. Hence, Ache mRNA in myoblasts shows rapid turnover, and upon differentiation, its level is increased by slowing the rate of mRNA degradation.
Department of Pharmacology 0636, University of California, San Diego, La Jolla 92093.
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D000110:Acetylcholinesterase / Q000235:genetics* / Q000378:metabolism; D000818:Animals; D002454:Cell Differentiation; D002460:Cell Line; D046508:Culture Techniques; D003513:Cycloheximide / Q000494:pharmacology; D015870:Gene Expression; D009124:Muscle Proteins / Q000235:genetics; D009132:Muscles / Q000166:cytology* / Q000378:metabolism / Q000502:physiology*; D018008:Myogenin; D011061:Poly A / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D011950:Receptors, Cholinergic / Q000235:genetics; D015534:Trans-Activators / Q000235:genetics; D014158:Transcription, Genetic
D009124:Muscle Proteins; D018008:Myogenin; D012333:RNA, Messenger; D011950:Receptors, Cholinergic; D015534:Trans-Activators; D011061:Poly A; D003513:Cycloheximide; D000110:Acetylcholinesterase