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  Control of CRK-RAC1 activity by the miR-1/206/133 miRNA family is essential for neuromuscular junction function

Klockner, I., Schutt, C., Gerhardt, T., Boettger, T., & Braun, T. (2022). Control of CRK-RAC1 activity by the miR-1/206/133 miRNA family is essential for neuromuscular junction function. NATURE COMMUNICATIONS, 13(1): 3180. doi:10.1038/s41467-022-30778-7.

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Klockner, Ina1, Author           
Schutt, Christian1, Author           
Gerhardt, Theresa1, Author           
Boettger, Thomas1, Author           
Braun, Thomas1, Author           
Affiliations:
1Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, Max Planck Society, ou_2591695              

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 Abstract: 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. The miR-1/133/206 gene family codes for the most abundant microRNAs in striated muscles. Here, Klockner et al show that inactivation of all family members in skeletal muscle prevents formation of normal neuromuscular junctions due to increased expression of the adaptor protein CRK.

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 Dates: 2022-06-08
 Publication Status: Published online
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 Identifiers: ISI: 000809119000013
DOI: 10.1038/s41467-022-30778-7
PMID: 35676269
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Title: NATURE COMMUNICATIONS
Source Genre: Journal
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Pages: - Volume / Issue: 13 (1) Sequence Number: 3180 Start / End Page: - Identifier: -