Phosphorylation of eIF2α Is a Translational Control Mechanism Regulating Muscle Stem Cell Quiescence and Self-Renewal

Cell Stem Cell. 2016 Jan 7;18(1):79-90. doi: 10.1016/j.stem.2015.09.020. Epub 2015 Nov 5.

Abstract

Regeneration of adult tissues depends on somatic stem cells that remain quiescent yet are primed to enter a differentiation program. The molecular pathways that prevent activation of these cells are not well understood. Using mouse skeletal muscle stem cells as a model, we show that a general repression of translation, mediated by the phosphorylation of translation initiation factor eIF2α at serine 51 (P-eIF2α), is required to maintain the quiescent state. Skeletal muscle stem cells unable to phosphorylate eIF2α exit quiescence, activate the myogenic program, and differentiate, but do not self-renew. P-eIF2α ensures in part the robust translational silencing of accumulating mRNAs that is needed to prevent the activation of muscle stem cells. Additionally, P-eIF2α-dependent translation of mRNAs regulated by upstream open reading frames (uORFs) contributes to the molecular signature of stemness. Pharmacological inhibition of eIF2α dephosphorylation enhances skeletal muscle stem cell self-renewal and regenerative capacity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Differentiation
  • Cell Proliferation
  • Eukaryotic Initiation Factor-2 / metabolism*
  • Female
  • Homozygote
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Muscle Fibers, Skeletal / metabolism*
  • Muscle, Skeletal / cytology*
  • Muscle, Skeletal / metabolism*
  • Myoblasts / metabolism
  • Open Reading Frames
  • Phosphorylation
  • RNA, Messenger / metabolism
  • Regeneration*
  • Satellite Cells, Skeletal Muscle / cytology*
  • Stem Cells / cytology*

Substances

  • Eukaryotic Initiation Factor-2
  • RNA, Messenger