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MATR3 is an endogenous inhibitor of DUX4 in FSHD muscular dystrophy. | LitMetric

MATR3 is an endogenous inhibitor of DUX4 in FSHD muscular dystrophy.

Cell Rep

Gene Expression and Muscular Dystrophy Unit, Division of Genetics and Cell Biology, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. Electronic address:

Published: September 2023

AI Article Synopsis

  • Facioscapulohumeral muscular dystrophy (FSHD) is a common neuromuscular disorder without a cure, linked to increased expression of the transcription factor DUX4, leading to muscle wasting.
  • MATR3, a protein associated with ALS and similar conditions, regulates DUX4 by binding to its DNA-binding domain, which helps protect muscle cells from DUX4's harmful effects.
  • Research suggests that a shorter form of MATR3 is effective in blocking DUX4 toxicity, positioning MATR3 as a potential target for FSHD treatment development.

Article Abstract

Facioscapulohumeral muscular dystrophy (FSHD) is one of the most common neuromuscular disorders and has no cure. Due to an unknown molecular mechanism, FSHD displays overlapping manifestations with the neurodegenerative disease amyotrophic lateral sclerosis (ALS). FSHD is caused by aberrant gain of expression of the transcription factor double homeobox 4 (DUX4), which triggers a pro-apoptotic transcriptional program resulting in inhibition of myogenic differentiation and muscle wasting. Regulation of DUX4 activity is poorly known. We identify Matrin 3 (MATR3), whose mutation causes ALS and dominant distal myopathy, as a cellular factor controlling DUX4 expression and activity. MATR3 binds to the DUX4 DNA-binding domain and blocks DUX4-mediated gene expression, rescuing cell viability and myogenic differentiation of FSHD muscle cells, without affecting healthy muscle cells. Finally, we characterize a shorter MATR3 fragment that is necessary and sufficient to directly block DUX4-induced toxicity to the same extent as the full-length protein. Collectively, our data suggest MATR3 as a candidate for developing a treatment for FSHD.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10591880PMC
http://dx.doi.org/10.1016/j.celrep.2023.113120DOI Listing

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