PUBLICATION
Connexin43 gap junctional intercellular communication inhibits evx1 expression and joint formation in regenerating fins
- Authors
- Bhattacharya, S., Hyland, C., Falk, M.M., Iovine, M.K.
- ID
- ZDB-PUB-200617-11
- Date
- 2020
- Source
- Development (Cambridge, England) 147(13): (Journal)
- Registered Authors
- Iovine, M. Kathryn
- Keywords
- Connexin43, GJIC, Skeletal regeneration, Zebrafish
- MeSH Terms
-
- Animal Fins/metabolism
- Cell Communication/physiology
- Gap Junctions/metabolism*
- Zebrafish
- Connexins/metabolism
- PubMed
- 32541014 Full text @ Development
Abstract
The gap junction protein Connexin43 (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 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 cx43lh10 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.
Genes / Markers
Figure Gallery (4 images)
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping