PUBLICATION
Overexpression of potassium channel Kcna5 alters skeletal patterning in the zebrafish regenerating fin
- Authors
- Seaver, A.W., Li, X., Iovine, M.K.
- ID
- ZDB-PUB-250906-8
- Date
- 2025
- Source
- Developmental Biology : (Journal)
- Registered Authors
- Iovine, M. Kathryn
- Keywords
- Cx43-GJIC, bioelectricity, regeneration, skeleton, zebrafish
- MeSH Terms
-
- Animal Fins*/embryology
- Animal Fins*/physiology
- Animals
- Animals, Genetically Modified
- Body Patterning*/genetics
- Body Patterning*/physiology
- Cell Communication
- Connexin 43/genetics
- Connexin 43/metabolism
- Gap Junctions/metabolism
- Gene Expression Regulation, Developmental
- HSP70 Heat-Shock Proteins/genetics
- HSP70 Heat-Shock Proteins/metabolism
- Joints/embryology
- Membrane Potentials
- Regeneration*/genetics
- Regeneration*/physiology
- Shaker Superfamily of Potassium Channels*/genetics
- Shaker Superfamily of Potassium Channels*/metabolism
- Zebrafish*/embryology
- Zebrafish*/genetics
- Zebrafish*/physiology
- Zebrafish Proteins*/genetics
- Zebrafish Proteins*/metabolism
- PubMed
- 40912447 Full text @ Dev. Biol.
Citation
Seaver, A.W., Li, X., Iovine, M.K. (2025) Overexpression of potassium channel Kcna5 alters skeletal patterning in the zebrafish regenerating fin. Developmental Biology. :.
Abstract
Skeletal patterning relies on a complex network of molecular and genetic regulators. However, our understanding of pathways governing joint placement and morphogenesis remains incomplete. Prior studies in have demonstrated that medially located Cx43 mediated gap junctional intercellular communication (GJIC) inhibits joint formation by the adjacent lateral skeletal precursor cells, and thereby determines skeletal patterning in the teleost regenerating fin. Here, we test the model that Cx43-GJIC regulates joint formation by propagating changes in membrane potential (ΔVm). To provide evidence that ΔVm is sufficient to influence joint formation, we generated a transgenic line that expresses the X. laevis voltage-gated channel, shaker-related subfamily, member 5 (kcna5) behind the temperature-inducible heat shock protein 70 (hsp70) promoter. Using this line, we demonstrate that Xl-kcna5 overexpression delays evx1 expression and causes longer segments. Moreover, the increased segment length in response to Xl-Kcna5 overexpression requires Cx43. These findings support a model whereby potassium channels act together with gap junction channels to influence joint formation, and therefore skeletal patterning, in the zebrafish regenerating fin.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping