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ETS transcription factor Erm controls subsynaptic gene expression in skeletal muscles.

Abstract：

:Accumulation of specific proteins at synaptic structures is essential for synapse assembly and function, but mechanisms regulating local protein enrichment remain poorly understood. At the neuromuscular junction (NMJ), subsynaptic nuclei underlie motor axon terminals within extrafusal muscle fibers and are transcriptionally distinct from neighboring nuclei. In this study, we show that expression of the ETS transcription factor Erm is highly concentrated at subsynaptic nuclei, and its mutation in mice leads to severe downregulation of many genes with normally enriched subsynaptic expression. Erm mutant mice display an expansion of the muscle central domain in which acetylcholine receptor (AChR) clusters accumulate, show gradual fragmentation of AChR clusters, and exhibit symptoms of muscle weakness mimicking congenital myasthenic syndrome (CMS). Together, our findings define Erm as an upstream regulator of a transcriptional program selective to subsynaptic nuclei at the NMJ and underscore the importance of transcriptional control of local synaptic protein accumulation.

journal_name

Neuron

journal_title

Neuron

authors

Hippenmeyer S,Huber RM,Ladle DR,Murphy K,Arber S

doi

10.1016/j.neuron.2007.07.028

subject

Has Abstract

pub_date

2007-09-06 00:00:00

pages

726-40

issue

5

eissn

0896-6273

issn

1097-4199

pii

S0896-6273(07)00573-9

journal_volume

55

pub_type

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