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MeCP2 deficiency promotes cell reprogramming by stimulating IGF1/AKT/mTOR signaling and activating ribosomal protein-mediated cell cycle gene translation Free
Wei Zhang 1 , Guihai Feng 1 , Libin Wang 1,2 , Fei Teng 1,2 , Liu Wang 1,2 , Wei Li 1,2 , Ying Zhang 1,* , and Qi Zhou 1,2,*
1 State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China
2 University of Chinese Academy of Sciences, Beijing 100049, China
*Correspondence to:* Correspondence to: Ying Zhang, E-mail: yingzhang@ioz.ac.cn; Qi Zhou, E-mail: zhouqi@ioz.ac.cn
J Mol Cell Biol, Volume 10, Issue 6, December 2018, Pages 515-526  https://doi.org/10.1093/jmcb/mjy018
Keyword: MeCP2, cell reprogramming, IGF1/AKT/mTOR signaling, ribosomal protein, cell cycle

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.