PUBLICATION

Connexin43 regulates joint location in zebrafish fins

Authors
Sims Jr, K., Eble, D.M., and Iovine, M.K.
ID
ZDB-PUB-090123-9
Date
2009
Source
Developmental Biology   327(2): 410-418 (Journal)
Registered Authors
Iovine, M. Kathryn
Keywords
Joint morphogenesis, Fin growth, Zebrafish, Gap junctions, Cx43, Short fin, Another long fin
MeSH Terms
  • Animals
  • Connexin 43/genetics
  • Connexin 43/metabolism*
  • Extremities/anatomy & histology*
  • Gene Expression Regulation, Developmental
  • In Situ Hybridization
  • Joints*/anatomy & histology
  • Joints*/embryology
  • Mesoderm/metabolism
  • Morphogenesis/physiology
  • Zebrafish/anatomy & histology*
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed
19150347 Full text @ Dev. Biol.
Abstract
Joints are essential for skeletal form and function, yet their development remains poorly understood. In zebrafish fins, joints form between the bony fin ray segments providing essentially unlimited opportunities to evaluate joint morphogenesis. Mutations in cx43 cause the short segment phenotype of short fin (sof(b123)) mutants, suggesting that direct cell-cell communication may regulate joint location. Interestingly, increased cx43 expression in the another long fin (alf(dty86)) mutant appears to cause joint failure typical of that mutant. Indeed, knockdown of cx43 in alf(dty86) mutant fins rescues joint formation. Together, these data reveal a correlation between the level of Cx43 expression in the fin ray mesenchyme and the location of joints. Cx43 was also observed laterally in cells associated with developing joints. Confocal microscopy revealed that the Cx43 protein initially surrounds the membranes of ZNS5-positive joint cells, but at later stages becomes polarized toward the underlying Cx43-positive mesenchymal cells. One possibility is that communication between the Cx43-positive mesenchyme and the overlying ZNS5-positive cells regulates joint location, and upregulation of Cx43 in joint-forming cells contributes to joint morphogenesis.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping