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Deficiency in the nuclear long noncoding RNA causes myogenic defects and heart remodeling in mice

Research output: Contribution to journalArticle

  • Monica Ballarino
  • Andrea Cipriano
  • Rossella Tita
  • Tiziana Santini
  • Fabio Desideri
  • Mariangela Morlando
  • Alessio Colantoni
  • Claudia Carrieri
  • Carmine Nicoletti
  • Antonio Musarò
  • Dònal O' Carroll
  • Irene Bozzoni

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Original languageEnglish
JournalEMBO Journal
Issue number18
Publication statusPublished - 14 Sep 2018


Myogenesis is a highly regulated process that involves the conversion of progenitor cells into multinucleated myofibers. Besides proteins and miRNAs, long noncoding RNAs (lncRNAs) have been shown to participate in myogenic regulatory circuitries. Here, we characterize a murine chromatin-associated muscle-specific lncRNA, Charme, which contributes to the robustness of the myogenic program in vitro and in vivo In myocytes, Charme depletion triggers the disassembly of a specific chromosomal domain and the downregulation of myogenic genes contained therein. Notably, several Charme-sensitive genes are associated with human cardiomyopathies and Charme depletion in mice results in a peculiar cardiac remodeling phenotype with changes in size, structure, and shape of the heart. Moreover, the existence of an orthologous transcript in human, regulating the same subset of target genes, suggests an important and evolutionarily conserved function for Charme Altogether, these data describe a new example of a chromatin-associated lncRNA regulating the robustness of skeletal and cardiac myogenesis.

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