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Mouse embryonic stem cells resist c-Jun induced differentiation when in suspension.

Authors
  • Wang, Bo1, 2, 3, 4
  • Li, Dongwei1, 2, 5, 6, 4
  • Chen, Jiekai1, 2, 5, 4
  • Liu, Jing1, 2, 4
  • Pei, Duanqing1, 2, 5, 4
  • 1 CAS Key Laboratory of Regenerative Biology, South China Institute for Stem Cell Biology and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou 510530, China. , (China)
  • 2 Guangdong Provincial Key Laboratory of Stem Cell and Regenerative Medicine, South China Institute for Stem Cell Biology and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou 510530, China. , (China)
  • 3 University of Chinese Academy of Sciences, China. , (China)
  • 4 GUANGZHOU Regenerative Medicine and Health Guangdong Laboratory, Guangzhou 510530, China. , (China)
  • 5 Guangzhou Branch of the Supercomputing Center of Chinese Academy of Sciences, Guangzhou 510530, China. , (China)
  • 6 CUHK-GIBH Joint Laboratory of Stem Cell and Regenerative Medicine, Chinese University of Hong Kong, Shatin, Hong Kong, China. , (China)
Type
Published Article
Journal
Cell regeneration (London, England)
Publication Date
Sep 01, 2018
Volume
7
Issue
1
Pages
16–21
Identifiers
DOI: 10.1016/j.cr.2018.05.002
PMID: 30671225
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

The oncogene c-Jun plays a key role in development and cancer. Yet, its role in cell fate decision remains poorly understood at the molecular level. Here we report that c-Jun confers different fate decisions upon mouse embryonic stem cells (mESCs) in adhesion vs suspension culture. We developed a Tet-on system for temporal induction of c-Jun expression by Doxycycline treatment in mESCs. We show that mESCs carrying the inducible c-Jun TetOn remain pluripotent and grow slowly in suspension when c-Jun expression is induced, whilst when the cells adhere they undergo differentiation and show normal proliferative potential upon c-Jun induction. Our data indicates that c-Jun pushes mESCs in suspension into cell cycle arrest at G1/S, by activating the cell cycle inhibitors Cdkn1a/b and Cdkn2/a/b/c. Despite this cell cycle arrest, they can still re-enter the cell cycle upon transfer to an adhesive surface, and grow into typical mESC colonies, albeit at a lower efficiency. These results demonstrate that mESCs respond to induced c-Jun overexpression differently in suspension or adherent cultures. Our results suggest that cells in suspension may be more resistant to differentiation than when they adhere.

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