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作 者:Jiakui Chen Gaofei Li Junwei Lian Ning Ma Zhibin Huang Jianchao Li Zilong Wen Wenqing Zhang Yiyue Zhang
机构地区:[1]Department of Developmental Biology,School of Basic Medical Sciences,Southern Medical University,Guangzhou 510515,China [2]Division of Cell,Developmental and Integrative Biology,School of Medicine,South China University of Technology,Guangzhou 510006,China [3]Division of Life Science,State Key Laboratory of Molecular Neuroscience,Hong Kong University of Science and Technology,Hong Kong,China
出 处:《Science China(Life Sciences)》2021年第12期2186-2201,共16页中国科学(生命科学英文版)
基 金:supported by the National Key Research and Development Program of China(2018YFA0800200);the National Natural Science Foundation of China(31922023);China Postdoctoral Science Foundation(2018M643071);Guangdong Province Universities and Colleges Pearl River Scholar Funded Scheme(2019);the Fundamental Research Funds for the Central Universities(2019ZD54 and 2019MS131)。
摘 要:Hematopoietic stem and progenitor cells(HSPCs)are able to self-renew and can give rise to all blood lineages throughout their lifetime,yet the mechanisms regulating HSPC development have yet to be discovered.In this study,we characterized a hematopoiesis defective zebrafish mutant line named smu07,which was obtained from our previous forward genetic screening,and found the HSPC expansion deficiency in the mutant.Positional cloning identified that slc20a1b,which encodes a sodium phosphate cotransporter,contributed to the smu07 blood phenotype.Further analysis demonstrated that mutation of slc20a1b affects HSPC expansion through cell cycle arrest at G2/M phases in a cell-autonomous manner.Our study shows that slc20a1b is a vital regulator for HSPC proliferation in zebrafish early hematopoiesis and provides valuable insights into HSPC development.
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