Control of CRK-RAC1 activity by the miR-1/206/133 miRNA family is essential for neuromuscular junction function.
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
08 06 2022
08 06 2022
Historique:
received:
03
06
2021
accepted:
07
05
2022
entrez:
8
6
2022
pubmed:
9
6
2022
medline:
11
6
2022
Statut:
epublish
Résumé
Formation and maintenance of neuromuscular junctions (NMJs) are essential for skeletal muscle function, allowing voluntary movements and maintenance of the muscle tone, thereby preventing atrophy. Generation of NMJs depends on the interaction of motor neurons with skeletal muscle fibers, which initiates a cascade of regulatory events that is essential for patterning of acetylcholine receptor (AChR) clusters at specific sites of the sarcolemma. Here, we show that muscle-specific miRNAs of the miR-1/206/133 family are crucial regulators of a signaling cascade comprising DOK7-CRK-RAC1, which is critical for stabilization and anchoring of postsynaptic AChRs during NMJ development and maintenance. We describe that posttranscriptional repression of CRK by miR-1/206/133 is essential for balanced activation of RAC1. Failure to adjust RAC1 activity severely compromises NMJ function, causing respiratory failure in neonates and neuromuscular symptoms in adult mice. We conclude that miR-1/206/133 serve a specific function for NMJs but are dispensable for skeletal muscle development.
Identifiants
pubmed: 35676269
doi: 10.1038/s41467-022-30778-7
pii: 10.1038/s41467-022-30778-7
pmc: PMC9178026
doi:
Substances chimiques
Crk protein, mouse
0
MicroRNAs
0
Proto-Oncogene Proteins c-crk
0
Receptors, Cholinergic
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
3180Informations de copyright
© 2022. The Author(s).
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