PUBLICATION

Deletion of Pr130 Interrupts Cardiac Development in Zebrafish

Authors
Yang, J., Li, Z., Gan, X., Zhai, G., Gao, J., Xiong, C., Qiu, X., Wang, X., Yin, Z., Zheng, F.
ID
ZDB-PUB-161116-2
Date
2016
Source
International Journal of Molecular Sciences   17(11): (Journal)
Registered Authors
Yin, Zhan, Zheng, Fang
Keywords
CRISPR-Cas9, cardiac development, pr130, zebrafish
MeSH Terms
  • Animals
  • Apoptosis
  • Gene Deletion
  • Heart/embryology*
  • Myocardial Contraction
  • Myocardium/enzymology
  • Myocardium/pathology
  • Myocytes, Cardiac/enzymology
  • Protein Phosphatase 2/genetics*
  • Zebrafish
PubMed
27845735 Full text @ Int. J. Mol. Sci.
Abstract
Protein phosphatase 2 regulatory subunit B, alpha (PPP2R3A), a regulatory subunit of protein phosphatase 2A (PP2A), is a major serine/threonine phosphatase that regulates crucial function in development and growth. Previous research has implied that PPP2R3A was involved in heart failure, and PR130, the largest transcription of PPP2R3A, functioning in the calcium release of sarcoplasmic reticulum (SR), plays an important role in the excitation-contraction (EC) coupling. To obtain a better understanding of PR130 functions in myocardium and cardiac development, two pr130-deletion zebrafish lines were generated using clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated proteins (Cas) system. Pr130-knockout zebrafish exhibited cardiac looping defects and decreased cardiac function (decreased fractional area and fractional shortening). Hematoxylin and eosin (H&E) staining demonstrated reduced cardiomyocytes. Subsequent transmission electron microscopy revealed that the bright and dark bands were narrowed and blurred, the Z- and M-lines were fogged, and the gaps between longitudinal myocardial fibers were increased. Additionally, increased apoptosis was observed in cardiomyocyte in pr130-knockout zebrafish compared to wild-type (WT). Taken together, our results suggest that pr130 is required for normal myocardium formation and efficient cardiac contractile function.
Genes / Markers
Figures
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Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes