Abstract:
:Myoblast fusion (MF) is required for muscle growth and repair, and its alteration contributes to muscle diseases. The mechanisms governing this process are incompletely understood, and no epigenetic regulator has been previously described. Ash1L is an epigenetic activator belonging to the Trithorax group of proteins and is involved in FSHD muscular dystrophy, autism and cancer. Its physiological role in skeletal muscle is unknown. Here we report that Ash1L expression is positively correlated with MF and reduced in Duchenne muscular dystrophy. In vivo, ex vivo and in vitro experiments support a selective and evolutionary conserved requirement for Ash1L in MF. RNA- and ChIP-sequencing indicate that Ash1L is required to counteract Polycomb repressive activity to allow activation of selected myogenesis genes, in particular the key MF gene Cdon. Our results promote Ash1L as an important epigenetic regulator of MF and suggest that its activity could be targeted to improve cell therapy for muscle diseases.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Castiglioni I,Caccia R,Garcia-Manteiga JM,Ferri G,Caretti G,Molineris I,Nishioka K,Gabellini Ddoi
10.1038/s41467-018-07313-8subject
Has Abstractpub_date
2018-11-28 00:00:00pages
5026issue
1issn
2041-1723pii
10.1038/s41467-018-07313-8journal_volume
9pub_type
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