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
  • Animals
  • Polymerase Chain Reaction
  • Genes, Essential
  • Sodium-Potassium-Exchanging ATPase/genetics*
  • Sodium-Potassium-Exchanging ATPase/metabolism
  • Heart/embryology*
  • Isoenzymes/genetics
  • Isoenzymes/metabolism
  • Embryo, Nonmammalian/physiology*
  • Zebrafish/embryology*
  • Mutation
  • Morphogenesis/physiology*
  • Molecular Sequence Data
  • In Situ Hybridization
  • DNA Primers
  • Gene Expression Regulation, Developmental
  • Heart Defects, Congenital/enzymology
  • Heart Defects, Congenital/genetics
  • Zebrafish Proteins/genetics*
  • Base Sequence
(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
No images available
Show all Figures
Expression
Phenotype
No data available
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
la1
    		Indel
    1 - 1 of 1
    Show
    Human Disease / Model
    No data available
    Sequence Targeting Reagents
    Target Reagent Reagent Type
    atp1a1a.1MO1-atp1a1a.1MRPHLNO
    atp1a2aMO1-atp1a2aMRPHLNO
    1 - 2 of 2
    Show
    Fish
    Antibodies
    Orthology
    Engineered Foreign Genes
    No data available
    Mapping
    Your Input Welcome
    We welcome your input and comments. Please use this form to recommend updates to the information in ZFIN. We appreciate as much detail as possible and references as appropriate. We will review your comments promptly.
    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.