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EphA7 regulates claudin6 and pronephros development in Xenopus

  1. Author:
    Sun, Jian
    Wang, Xiaolei
    Shi, Yu
    Li, Jiejing
    Li, Chaocui
    Shi, Zhaoying
    Chen, Yonglong
    Mao, Bingyu

  2. Author Address

    Chinese Acad Sci, Kunming Inst Zool, State Key Lab Genet Resources & Evolut, Kunming, Yunnan, Peoples R China.Southern Univ Sci & Technol, Dept Biol, Shenzhen Key Lab Cell Microenvironm, Shenzhen, Guangdong, Peoples R China.Chongqing Med Univ, Childrens Hosp, Dept Clin Lab, Chongqing, Peoples R China.NCI, Canc & Dev Biol Lab, NIH, Frederick, MD 21702 USA.
    1. Year: 2018
    2. Date: Jan 8
  2. Journal: Biochemical and Biophysical Research Communications
  3. ACADEMIC PRESS INC ELSEVIER SCIENCE,
    1. 495
    2. 2
    3. Pages: 1580-1587
  5. Type of Article: Article
  6. ISSN: 0006-291X
  1. Abstract:

    Eph/ephrin molecules are widely expressed during embryonic development, and function in a variety of developmental processes. Here we studied the roles of the Eph receptor EphA7 and its soluble form in Xenopus pronephros development. EphA7 is specifically expressed in pronephric tubules at tadpole stages and knockdown of EphA7 by a translation blocking morpholino led to defects in tubule cell differentiation and morphogenesis. A soluble form of EphA7 (sEphA7) was also identified. Interestingly, the membrane level of claudin6 (CLDN6), a tetraspan transmembrane tight junction protein, was dramatically reduced in the translation blocking morpholino injected embryos, but not when a splicing morpholino was used, which blocks only the full length EphA7. In cultured cells, EphA7 binds and phosphorylates CLDN6, and reduces its distribution at the cell surface. Our work suggests a role of EphA7 in the regulation of cell adhesion during pronephros development, whereas sEphA7 works as an antagonist. (C) 2017 Elsevier Inc. All rights reserved.

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External Sources

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  2. DOI: 10.1016/j.bbrc.2017.12.027
  3. PMID: 29223398
  4. View record in Web of Science®
  5. WOS: 000424732700002

Library Notes

  1. Fiscal Year: FY2017-2018
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