MicroRNAs coordinate an alternative splicing network during mouse postnatal heart development

Genes Dev. 2010 Apr 1;24(7):653-8. doi: 10.1101/gad.1894310. Epub 2010 Mar 18.

Abstract

Alternative splicing transitions have been identified recently as a conserved component of vertebrate heart remodeling during postnatal development. Here we report that the targeted deletion of Dicer, specifically in adult mouse myocardium, reveals the role of microRNAs (miRNAs) in regulating networks of postnatal splicing transitions and in maintaining adult splicing programs. We demonstrate a direct role for miR-23a/b in the dramatic postnatal down-regulation of CUGBP and ETR-3-like factor (CELF) proteins that regulate nearly half of developmentally regulated splicing transitions in the heart. These findings define a hierarchy in which rapid postnatal up-regulation of specific miRNAs controls expression of alternative splicing regulators and the subsequent splicing transitions of their downstream targets.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alternative Splicing / physiology*
  • Animals
  • CELF1 Protein
  • Cell Line
  • DEAD-box RNA Helicases / genetics
  • Down-Regulation
  • Endoribonucleases / genetics
  • Gene Knockdown Techniques
  • Heart / growth & development*
  • Mice
  • MicroRNAs / antagonists & inhibitors
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • RNA-Binding Proteins / metabolism
  • Ribonuclease III
  • Up-Regulation

Substances

  • CELF1 Protein
  • CELF1 protein, mouse
  • MicroRNAs
  • Mirn23b microRNA, mouse
  • RNA-Binding Proteins
  • Endoribonucleases
  • Dicer1 protein, mouse
  • Ribonuclease III
  • DEAD-box RNA Helicases