PUBLICATION
Zebrafish short fin mutations in connexin43 lead to aberrant gap junctional intercellular communication
- Authors
- Hoptak-Solga, A.D., Klein, K.A., Derosa, A.M., White, T.W., and Iovine, M.K.
- ID
- ZDB-PUB-070711-16
- Date
- 2007
- Source
- FEBS letters 581(17): 3297-3302 (Journal)
- Registered Authors
- Iovine, M. Kathryn
- Keywords
- Gap junction, Cx43, Bone growth, Zebrafish, short fin
- MeSH Terms
-
- Connexin 43/genetics*
- Zebrafish/genetics*
- Bones of Lower Extremity/abnormalities
- Gap Junctions/genetics*
- Mutation, Missense/physiology
- Humans
- Zebrafish Proteins/genetics*
- HeLa Cells
- Animals
- Patch-Clamp Techniques
- Cell Communication/genetics*
- Phenotype
- Transfection
- Limb Deformities, Congenital/genetics*
- PubMed
- 17599838 Full text @ FEBS Lett.
Citation
Hoptak-Solga, A.D., Klein, K.A., Derosa, A.M., White, T.W., and Iovine, M.K. (2007) Zebrafish short fin mutations in connexin43 lead to aberrant gap junctional intercellular communication. FEBS letters. 581(17):3297-3302.
Abstract
Mutations in the zebrafish connexin43 (cx43) gene cause the short fin phenotype, indicating that direct cell-cell communication contributes to bone length. Three independently generated cx43 alleles exhibit short segments of variable sizes, suggesting that gap junctional intercellular communication may regulate bone growth. Dye coupling assays showed that all alleles are capable of forming gap junction channels. However, ionic coupling assays revealed allele-specific differences in coupling efficiency and gating. For instance, oocyte pairs expressing the weakest allele exhibited much higher levels of coupling than either of the strong alleles. Therefore, measurable differences in Cx43 function may be correlated with the severity of defects in bone length.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping