MeCP2 deficiency promotes cell reprogramming by stimulating IGF1/AKT/mTOR signaling and activating ribosomal protein-mediated cell cycle gene translation

J Mol Cell Biol. 2018 Dec 1;10(6):515-526. doi: 10.1093/jmcb/mjy018.

Abstract

The generation of induced pluripotent stem cells (iPSCs) offers a great opportunity in research and regenerative medicine. The current poor efficiency and incomplete mechanistic understanding of the reprogramming process hamper the clinical application of iPSCs. MeCP2 connects histone modification and DNA methylation, which are key changes of somatic cell reprogramming. However, the role of MeCP2 in cell reprogramming has not been examined. In this study, we found that MeCP2 deficiency enhanced reprogramming efficiency and stimulated cell proliferation through regulating cell cycle protein expression in the early stage of reprogramming. MeCP2 deficiency enhanced the expression of ribosomal protein genes, thereby enhancing reprogramming efficiency through promoting the translation of cell cycle genes. In the end, MeCP2 deficiency stimulated IGF1/AKT/mTOR signaling and activated ribosomal protein gene expression. Taken together, our data indicate that MeCP2 deficiency promoted cell reprogramming through stimulating IGF1/AKT/mTOR signaling and activating ribosomal protein-mediated cell cycle gene translation in the early stage of reprogramming.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Cycle
  • Cells, Cultured
  • Cellular Reprogramming*
  • Female
  • Gene Deletion
  • Insulin-Like Growth Factor I / metabolism*
  • Methyl-CpG-Binding Protein 2 / genetics*
  • Methyl-CpG-Binding Protein 2 / metabolism
  • Mice
  • Protein Biosynthesis
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Ribosomal Proteins / genetics*
  • Signal Transduction*
  • TOR Serine-Threonine Kinases / metabolism*

Substances

  • Mecp2 protein, mouse
  • Methyl-CpG-Binding Protein 2
  • Ribosomal Proteins
  • insulin-like growth factor-1, mouse
  • Insulin-Like Growth Factor I
  • mTOR protein, mouse
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases