PUBLICATION

Na,K-ATPase is essential for embryonic heart development in the zebrafish

Authors
Shu, X., Cheng, K., Patel, N., Chen, F., Joseph, E., Tsai, H.-J., and Chen, J.-N.
ID
ZDB-PUB-031111-8
Date
2003
Source
Development (Cambridge, England)   130: 6165-6173 (Journal)
Registered Authors
Chen, Jau-Nian, Joseph, Elaine, Shu, Xiaodong, Tsai, Huai-Jen
Keywords
heart development, zebrafish, Na,K-ATPase
MeSH Terms
  • Zebrafish/embryology*
  • Mutation
  • Heart Defects, Congenital/enzymology
  • Heart Defects, Congenital/genetics
  • Sodium-Potassium-Exchanging ATPase/genetics*
  • Sodium-Potassium-Exchanging ATPase/metabolism
  • Gene Expression Regulation, Developmental
  • Heart/embryology*
  • Morphogenesis/physiology*
  • Genes, Essential
  • Isoenzymes/genetics
  • Isoenzymes/metabolism
  • Animals
  • DNA Primers
  • Zebrafish Proteins/genetics*
  • Polymerase Chain Reaction
  • In Situ Hybridization
  • Base Sequence
  • Molecular Sequence Data
  • Embryo, Nonmammalian/physiology*
(all 20)
PubMed
14602677 Full text @ Development
Abstract
Na,K-ATPase is an essential gene maintaining electrochemical gradients across the plasma membrane. Although previous studies have intensively focused on the role of Na,K-ATPase in regulating cardiac function in the adults, little is known about the requirement for Na,K-ATPase during embryonic heart development. Here, we report the identification of a zebrafish mutant, heart and mind, which exhibits multiple cardiac defects, including the primitive heart tube extension abnormality, aberrant cardiomyocyte differentiation, and reduced heart rate and contractility. Molecular cloning reveals that the heart and mind lesion resides in the alpha1B1 isoform of Na,K-ATPase. Blocking Na,K-ATPase alpha1B1 activity by pharmacological means or by morpholino antisense oligonucleotides phenocopies the patterning and functional defects of heart and mind mutant hearts, suggesting crucial roles for Na,K-ATPase alpha1B1 in embryonic zebrafish hearts. In addition to alpha1B1, the Na,K-ATPase alpha2 isoform is required for embryonic cardiac patterning. Although the alpha1B1 and alpha2 isoforms share high degrees of similarities in their coding sequences, they have distinct roles in patterning zebrafish hearts. The phenotypes of heart and mind mutants can be rescued by supplementing alpha1B1, but not alpha2, mRNA to the mutant embryos, demonstrating that alpha1B1 and alpha2 are not functionally equivalent. Furthermore, instead of interfering with primitive heart tube formation or cardiac chamber differentiation, blocking the translation of Na,K-ATPase alpha2 isoform leads to cardiac laterality defects.
Genes / Markers
Figures
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Expression
Gene Antibody Fish Conditions Stage Qualifier Anatomy Assay Figure
atp1a1a.1atp1a1a.1la1/la1 (EKW)standard conditionsLong-pecISH
atp1a1a.1WTstandard conditionsLong-pecISH
irx1batp1a1a.1la1/la1 (EKW)standard conditionsLong-pecISH
irx1bWTstandard conditionsLong-pecISH
myh7atp1a1a.1la1/la1 (EKW)standard conditionsPrim-5ISH
myh7atp1a1a.1la1/la1 (EKW)standard conditionsLong-pecISH
myh7WTstandard conditionsLong-pecISH
myh7WTstandard conditionsPrim-5ISH
vcanaatp1a1a.1la1/la1 (EKW)standard conditionsLong-pecISH
vcanaWTstandard conditionsLong-pecISH
1 - 10 of 10
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Phenotype
No data available
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
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Citation
Shu, X., Cheng, K., Patel, N., Chen, F., Joseph, E., Tsai, H.-J., and Chen, J.-N. (2003) Na,K-ATPase is essential for embryonic heart development in the zebrafish. Development (Cambridge, England). 130:6165-6173.