PUBLICATION
Connexin43 (GJA1) is required in the population of dividing cells during fin regeneration
- Authors
- Hoptak-Solga, A.D., Nielsen, S., Jain, I., Thummel, R., Hyde, D.R., and Iovine, M.K.
- ID
- ZDB-PUB-080415-14
- Date
- 2008
- Source
- Developmental Biology 317(2): 541-548 (Journal)
- Registered Authors
- Hyde, David R., Iovine, M. Kathryn, Thummel, Ryan
- Keywords
- Bone growth, short fin, Regeneration, Zebrafish, Cell proliferation, Cx43, GJIC
- MeSH Terms
-
- Animal Structures/physiology*
- Animals
- Cell Communication/physiology*
- Cell Proliferation
- Connexin 43/genetics
- Connexin 43/metabolism*
- Cryoultramicrotomy
- Electroporation
- Gap Junctions/physiology*
- Immunoblotting
- In Situ Hybridization
- Mutation/genetics
- Regeneration/physiology*
- Zebrafish/genetics*
- Zebrafish/physiology
- PubMed
- 18406403 Full text @ Dev. Biol.
Citation
Hoptak-Solga, A.D., Nielsen, S., Jain, I., Thummel, R., Hyde, D.R., and Iovine, M.K. (2008) Connexin43 (GJA1) is required in the population of dividing cells during fin regeneration. Developmental Biology. 317(2):541-548.
Abstract
In zebrafish, mutations in the gap junction gene connexin43 lead to short bony fin ray segments that give rise to the short fin phenotype. The sof(b123) mutant exhibits fins that are half the length of wild-type fins and have reduced levels of cx43 mRNA. We find that sof(b123) regenerating fins exhibit reduced levels of cell proliferation. Interestingly, the number of dividing cells per unit length of fin growth is similar between wild-type and mutant fins, suggesting that the number of cells that enter the cell cycle is specifically affected in sof(b123). Expression of cx43 is identified in mitotic cells, which further suggests that Cx43 may contribute to establishing or maintaining the population of dividing cells. Indeed, missense alleles exhibiting high or low levels of gap junctional communication reveal a correlation between defects in direct cell-cell communication, cell proliferation, and segment length. Finally, targeted gene knockdown of cx43 in adult regenerating fins recapitulates the sof(b123) phenotype, revealing that the loss of Cx43 is sufficient to reduce both cell proliferation and segment length. We hypothesize that the level of gap junctional intercellular communication among dividing cells regulates the level of cell proliferation and ultimately regulates bone growth.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping