Med23 serves as a gatekeeper of the myeloid potential of hematopoietic stem cells

Xufeng Chen, Jingyao Zhao, Chan Gu, Yu Cui, Yuling Dai, Guangrong Song, Haifeng Liu, Hao Shen, Yuanhua Liu, Yuya Wang, Huayue Xing, Xiaoyan Zhu, Pei Hao, Fan Guo () and Xiaolong Liu ()
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Xufeng Chen: Chinese Academy of Sciences
Jingyao Zhao: Chinese Academy of Sciences
Chan Gu: Sichuan University
Yu Cui: Chinese Academy of Sciences
Yuling Dai: Chinese Academy of Sciences
Guangrong Song: ShanghaiTech University
Haifeng Liu: Chinese Academy of Sciences
Hao Shen: Chinese Academy of Sciences
Yuanhua Liu: Chinese Academy of Sciences
Yuya Wang: Chinese Academy of Sciences
Huayue Xing: Chinese Academy of Sciences
Xiaoyan Zhu: Chinese Academy of Sciences
Pei Hao: Chinese Academy of Sciences
Fan Guo: Sichuan University
Xiaolong Liu: Chinese Academy of Sciences

Nature Communications, 2018, vol. 9, issue 1, 1-12

Abstract: Abstract In response to myeloablative stresses, HSCs are rapidly activated to replenish myeloid progenitors, while maintaining full potential of self-renewal to ensure life-long hematopoiesis. However, the key factors that orchestrate HSC activities during physiological stresses remain largely unknown. Here we report that Med23 controls the myeloid potential of activated HSCs. Ablation of Med23 in hematopoietic system leads to lymphocytopenia. Med23-deficient HSCs undergo myeloid-biased differentiation and lose the self-renewal capacity. Interestingly, Med23-deficient HSCs are much easier to be activated in response to physiological stresses. Mechanistically, Med23 plays essential roles in maintaining stemness genes expression and suppressing myeloid lineage genes expression. Med23 is downregulated in HSCs and Med23 deletion results in better survival under myeloablative stress. Altogether, our findings identify Med23 as a gatekeeper of myeloid potential of HSCs, thus providing unique insights into the relationship among Med23-mediated transcriptional regulations, the myeloid potential of HSCs and HSC activation upon stresses.

Date: 2018
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DOI: 10.1038/s41467-018-06282-2

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