例如:"lncRNA", "apoptosis", "WRKY"

Connexin 43 gap junctional intercellular communication inhibits evx1 expression and joint formation in regenerating fins.

Development. 2020 Jul 03;147(13)
Shashwati Bhattacharya 1 , Caitlin Hyland 2 , Matthias M Falk 2 , M Kathryn Iovine 1
Shashwati Bhattacharya 1 , Caitlin Hyland 2 , Matthias M Falk 2 , M Kathryn Iovine 1

[No authors listed]

Author information
  • 1 Department of Biological Sciences, Lehigh University, Bethlehem, PA 18020, USA mki3@lehigh.edu shb215@lehigh.edu.
  • 2 Department of Biological Sciences, Lehigh University, Bethlehem, PA 18020, USA.

摘要


The gap junction protein Connexin 43 (Cx43) contributes to cell fate decisions that determine the location of fin ray joints during regeneration. Here, we provide insights into how Cx43, expressed medially, influences changes in gene expression in lateral skeletal precursor cells. Using the Gap27 peptide inhibitor specific to Cx43, we show that Cx43-gap junctional intercellular communication (GJIC) influences Cx43-dependent skeletal phenotypes, including segment length. We also demonstrate that Cx43-GJIC influences the expression of the Smp/β-catenin pathway in the lateral skeletal precursor cells, and does not influence the Sema3d pathway. Moreover, we show that the cx43 allele, which has increased Cx43 protein levels, exhibits increased regenerate length and segment length. These phenotypes are rescued by Gap27, suggesting that increased Cx43 is responsible for the observed Cx43 phenotypes. Finally, our findings suggest that inhibition of Cx43 hemichannel activity does not influence Cx43-dependent skeletal phenotypes. These data provide evidence that Cx43-GJIC is responsible for regulating cell fate decisions associated with appropriate joint formation in the regenerating fin.

KEYWORDS: Connexin 43, GJIC, Skeletal regeneration, Zebrafish