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The m6A methyltransferase METTL3 regulates muscle maintenance and growth in mice

Petrosino, Jennifer M. ; Hinger, Scott A. ; Golubeva, Volha A. ; Barajas, Juan M. ; Dorn, Lisa E. ; Iyer, Chitra C. ; Sun, Hui-Lung ; Arnold, W. David ; He, Chuan ; Accornero, Federica

Nature communications, 2022-01, Vol.13 (1), p.168-168, Article 168 [Periódico revisado por pares]

London: Nature Publishing Group

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Título:
The m6A methyltransferase METTL3 regulates muscle maintenance and growth in mice
Autor: Petrosino, Jennifer M. ; Hinger, Scott A. ; Golubeva, Volha A. ; Barajas, Juan M. ; Dorn, Lisa E. ; Iyer, Chitra C. ; Sun, Hui-Lung ; Arnold, W. David ; He, Chuan ; Accornero, Federica
Assuntos: Activin ; Atrophy ; Eutrophication ; Fluctuations ; Gene expression ; Genomes ; Homeostasis ; Hypertrophy ; Methyltransferase ; Muscles ; Musculoskeletal system ; Myostatin ; N6-methyladenosine ; Overloading ; Phenotypes ; Post-transcription ; Proteomes ; Signaling ; Skeletal muscle
É parte de: Nature communications, 2022-01, Vol.13 (1), p.168-168, Article 168
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Descrição: Abstract Skeletal muscle serves fundamental roles in organismal health. Gene expression fluctuations are critical for muscle homeostasis and the response to environmental insults. Yet, little is known about post-transcriptional mechanisms regulating such fluctuations while impacting muscle proteome. Here we report genome-wide analysis of mRNA methyladenosine (m 6 A) dynamics of skeletal muscle hypertrophic growth following overload-induced stress. We show that increases in METTL3 (the m 6 A enzyme), and concomitantly m 6 A, control skeletal muscle size during hypertrophy; exogenous delivery of METTL3 induces skeletal muscle growth, even without external triggers. We also show that METTL3 represses activin type 2 A receptors (ACVR2A) synthesis, blunting activation of anti-hypertrophic signaling. Notably, myofiber-specific conditional genetic deletion of METTL3 caused spontaneous muscle wasting over time and abrogated overload-induced hypertrophy; a phenotype reverted by co-administration of a myostatin inhibitor. These studies identify a previously unrecognized post-transcriptional mechanism promoting the hypertrophic response of skeletal muscle via control of myostatin signaling.
Editor: London: Nature Publishing Group
Idioma: Inglês

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The m6A methyltransferase METTL3 regulates muscle maintenance and growth in mice

Petrosino, Jennifer M. ; Hinger, Scott A. ; Golubeva, Volha A. ; Barajas, Juan M. ; Dorn, Lisa E. ; Iyer, Chitra C. ; Sun, Hui-Lung ; Arnold, W. David ; He, Chuan ; Accornero, Federica

London: Nature Publishing Group

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