Basic & Clinical Medicine ›› 2020, Vol. 40 ›› Issue (7): 948-954.

• Original Articles • Previous Articles     Next Articles

Role of ZBED3 in cortex cerebral development through conventional Zbed3 knockout mouse

SUN Chang-jie1, SHU Peng-cheng1, PENG Xiao-zhong1,2*   

  1. 1. State Key Laboratory of Medical Molecular Biology, Department of Molecular and Biochemistry, Medical Primate Research Center, Neuroscience Center, Institute of Basic Medical Sciences CAMS, School of Basic Medicine PUMC, Beijing 100005;
    2. Institute of Medical Biology CAMS, Kunming 650118, China
  • Received:2020-05-14 Revised:2020-05-17 Online:2020-07-05 Published:2020-06-29
  • Contact: *pengxiaozhong@pumc.edu.cn

Abstract: Objective To explore the role of zinc finger BED domain-containing protein 3, a member of zinc finger domain protein superfamily, in cortex cerebral development through conventional Zbed3 knockout mouse. Methods In situ hybridization and immunofluorescence were used to detect the mRNA and protein of Zbed3. Immunofluorescence was recruited to analyze the proliferation of neural progenitor cells in Zbed3 conventional knockout mouse. EdU labeling and immunofluorescence were used to analyze the neural position and layer fates in Zbed3 conven-tional knockout mouse. RT-qPCR and Western blot were used to detect the gene expression difference caused by Zbed3 knockout. Results Zbed3 mRNA and protein were not found in Zbed3 conventional knockout mouse; Knockout of Zbed3 failed to affect the proliferation of neural progenitor cells and the formation of neocortex layers. The expression of β-catenin was up-regulated in Zbed3 conventional knockout mouse. Conclusions Knockout of Zbed3 is not able to cause the apparent phenotype in cortex cerebral development.

Key words: Zbed3, cortex cerebral development, canonical Wnt signaling pathway, β-catenin

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