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Nerve-Dependent Induction of AChR ϵ-Subunit Gene Expression in Muscle Is Independent of State of Differentiation

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Brenner,  Hans R.
Max Planck Society;

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Kues,  Winfried
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Witzemann,  Veit
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;
Working Group Witzemann / Koenen, Max Planck Institute for Medical Research, Max Planck Society;
Molecular anatomy of the neuromuscular junction, Max Planck Institute for Medical Research, Max Planck Society;
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Sakmann,  Bert
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Brenner, H. R., Rotzler, S., Kues, W., Witzemann, V., & Sakmann, B. (1994). Nerve-Dependent Induction of AChR ϵ-Subunit Gene Expression in Muscle Is Independent of State of Differentiation. Developmental Biology, 165(2), 527-536. doi:10.1006/dbio.1994.1272.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0019-A99C-8
Abstract
To determine if the expression of the ϵ-subunit of the acetylcholine receptor by the subsynaptic nuclei in skeletal muscle is dependent on the state of differentiation of the muscle, we have compared the spatiotemporal distribution of ϵ-subunit transcripts during synapse formation in fetal and adult muscle. Both during "ontogenic" synaptogenesis in the fetus and during "ectopic" synaptogenesis in the adult animal the motor nerve induced locally the expression of the ϵ-subunit mRNA in subsynaptic nuclei. The temporal expression patterns at both types of developing synapses were similar. The results support the view that in muscle developing in vivo ϵ-subunit gene transcription and its stabilization in subsynaptic nuclei is exclusively controlled by the motor neuron, independently of the developmental state of the muscle nuclei. Thus, both nerve and muscle remain plastic in their respective abilities to induce and express the synapse-specific combination of AChR subunit genes.