Dax1 and Nanog act in parallel to stabilize mouse embryonic stem cells and induced pluripotency

Junlei Zhang, Gaoke Liu, Yan Ruan, Jiali Wang, Ke Zhao, Ying Wan, Bing Liu, Hongting Zheng, Tao Peng, Wei Wu, Ping He, Fu-Quan Hu () and Rui Jian ()
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Junlei Zhang: Third Military Medical University
Gaoke Liu: Third Military Medical University
Yan Ruan: Third Military Medical University
Jiali Wang: Third Military Medical University
Ke Zhao: Laboratory of Oncology, Affiliated Hospital of Academy of Military Medical Sciences
Ying Wan: Biomedical Analysis Center, Third Military Medical University
Bing Liu: Laboratory of Oncology, Affiliated Hospital of Academy of Military Medical Sciences
Hongting Zheng: Xinqiao Hospital, Third Military Medical University
Tao Peng: Research Center of Laboratory Medicine, Chengdu Military General Hospital
Wei Wu: Southwest Hospital, Third Military Medical University
Ping He: Southwest Hospital, Third Military Medical University
Fu-Quan Hu: Third Military Medical University
Rui Jian: Third Military Medical University

Nature Communications, 2014, vol. 5, issue 1, 1-16

Abstract: Abstract Nanog expression is heterogeneous and dynamic in embryonic stem cells (ESCs). However, the mechanism for stabilizing pluripotency during the transitions between Nanoghigh and Nanoglow states is not well understood. Here we report that Dax1 acts in parallel with Nanog to regulate mouse ESC (mESCs) identity. Dax1 stable knockdown mESCs are predisposed towards differentiation but do not lose pluripotency, whereas Dax1 overexpression supports LIF-independent self-renewal. Although partially complementary, Dax1 and Nanog function independently and cannot replace one another. They are both required for full reprogramming to induce pluripotency. Importantly, Dax1 is indispensable for self-renewal of Nanoglow mESCs. Moreover, we report that Dax1 prevents extra-embryonic endoderm (ExEn) commitment by directly repressing Gata6 transcription. Dax1 may also mediate inhibition of trophectoderm differentiation independent or as a downstream effector of Oct4. These findings establish a basal role of Dax1 in maintaining pluripotency during the state transition of mESCs and somatic cell reprogramming.

Date: 2014
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DOI: 10.1038/ncomms6042

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