Deficiency of microRNA <i>miR-34a</i> expands cell fate potential in pluripotent stem cells

Yong Jin Choi(Institut de Biologie Moléculaire et Cellulaire), Chao‐Po Lin(Institut de Biologie Moléculaire et Cellulaire), Davide Risso(University of California, Berkeley), Sean Chen(Institut de Biologie Moléculaire et Cellulaire), Thomas A. Kim(Institut de Biologie Moléculaire et Cellulaire), Meng How Tan(Stanford University), Jin Billy Li(Stanford University), Yalei Wu(Thermo Fisher Scientific (United States)), Caifu Chen(Integrated DNA Technologies (United States)), Zhenyu Xuan(The University of Texas at Dallas), Todd S. Macfarlan(Eunice Kennedy Shriver National Institute of Child Health and Human Development), Weiqun Peng(George Washington University), K. C. Kent Lloyd(University of California, Davis), Sang Yong Kim(New York University), Terence P. Speed(The University of Melbourne), Lin He(Institut de Biologie Moléculaire et Cellulaire)
Science
January 12, 2017
10.1126/science.aag1927
Cited by 159Open Access
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Abstract

Limiting potential for totipotency Biological roles for microRNAs are not limited to RNA silencing and posttranscriptional regulation; they have now been shown to also regulate cell pluripotency. Choi et al. eliminated miR-34a from mouse embryonic stem cells and found that the cells exhibited a bidirectional cell fate potential, generating both embryonic and extraembryonic lineages (see the Perspective by Hasuwa and Siomi). During miR-34a deficiency, an endogenous retrovirus was induced, at least in part through Gata2-dependent transcriptional activation. Thus, the interplay of protein-coding genes, noncoding RNAs, and endogenous retroviruses can change cell fate plasticity and the developmental potential of pluripotent stem cells. Science , this issue p. eaag1927 ; see also p. 581

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