MicroRNA-222 regulates muscle alternative splicing through Rbm24 during differentiation of skeletal muscle cells

Cell Death Dis. 2016 Feb 4;7(2):e2086. doi: 10.1038/cddis.2016.10.

Abstract

A number of microRNAs have been shown to regulate skeletal muscle development and differentiation. MicroRNA-222 is downregulated during myogenic differentiation and its overexpression leads to alteration of muscle differentiation process and specialized structures. By using RNA-induced silencing complex (RISC) pulldown followed by RNA sequencing, combined with in silico microRNA target prediction, we have identified two new targets of microRNA-222 involved in the regulation of myogenic differentiation, Ahnak and Rbm24. Specifically, the RNA-binding protein Rbm24 is a major regulator of muscle-specific alternative splicing and its downregulation by microRNA-222 results in defective exon inclusion impairing the production of muscle-specific isoforms of Coro6, Fxr1 and NACA transcripts. Reconstitution of normal levels of Rbm24 in cells overexpressing microRNA-222 rescues muscle-specific splicing. In conclusion, we have identified a new function of microRNA-222 leading to alteration of myogenic differentiation at the level of alternative splicing, and we provide evidence that this effect is mediated by Rbm24 protein.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alternative Splicing
  • Cell Differentiation / physiology
  • Humans
  • MicroRNAs / genetics*
  • MicroRNAs / metabolism
  • Muscle Development
  • Muscle Fibers, Skeletal / cytology*
  • Muscle Fibers, Skeletal / metabolism
  • RNA-Binding Proteins / genetics*
  • RNA-Binding Proteins / metabolism

Substances

  • MIRN222 microRNA, human
  • MicroRNAs
  • RBM24 protein, human
  • RNA-Binding Proteins