ZFIN ID: ZDB-PUB-201215-12
Kcnb1 plays a role in development of the inner ear
Jedrychowska, J., Gasanov, E.V., Korzh, V.
Date: 2020
Source: Developmental Biology   471: 65-75 (Journal)
Registered Authors: Korzh, Vladimir
Keywords: Brain ventricular system, Cilia, Ear, Kinocilium, Kv channels, Otolith formation, Voltage-gated potassium channels, Zebrafish
MeSH Terms:
  • Animals
  • Cell Proliferation*
  • Cilia/genetics
  • Cilia/metabolism
  • Ear, Inner/embryology*
  • Loss of Function Mutation
  • Mechanotransduction, Cellular*
  • Potassium Channels, Voltage-Gated/genetics
  • Potassium Channels, Voltage-Gated/metabolism*
  • Protein Transport/genetics
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed: 33316259 Full text @ Dev. Biol.
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ABSTRACT
The function of the inner ear depends on the maintenance of high concentrations of K+ ions. The slow-inactivating delayed rectifier Kv2.1/KCNB1 channel works in the inner ear in mammals. The kcnb1 gene is expressed in the otic vesicle of developing zebrafish, suggesting its role in development of the inner ear. In the present study, we found that a Kcnb1 loss-of-function mutation affected development of the inner ear at multiple levels, including otic vesicle expansion, otolith formation, and the proliferation and differentiation of mechanosensory cells. This resulted in defects of kinocilia and stereocilia and abnormal function of the inner ear detected by behavioral assays. The quantitative transcriptional analysis of 75 genes demonstrated that the kcnb1 mutation affected the transcription of genes that are involved in K+ metabolism, cell proliferation, cilia development, and intracellular protein trafficking. These results demonstrate a role for Kv2.1/Kcnb1 channels in development of the inner ear in zebrafish.
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