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Int. J. Mol. Sci. 2016, 17(11), 1746; doi:10.3390/ijms17111746

Deletion of Pr130 Interrupts Cardiac Development in Zebrafish

1
Center for Gene Diagnosis, Zhongnan Hospital of Wuhan University, Wuhan 430071, China
2
Department of Cardiology, Zhongnan Hospital of Wuhan University, Wuhan 430071, China
3
Key Laboratory of Aquatic Biodiversity and Conservation of Chinese Academy of Sciences, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan 430072, China
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Academic Editor: Li Lin
Received: 20 August 2016 / Revised: 10 October 2016 / Accepted: 13 October 2016 / Published: 11 November 2016
(This article belongs to the Section Molecular Pathology, Diagnostics, and Therapeutics)
View Full-Text   |   Download PDF [6013 KB, uploaded 11 November 2016]   |  

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. View Full-Text
Keywords: CRISPR-Cas9; pr130; cardiac development; zebrafish CRISPR-Cas9; pr130; cardiac development; zebrafish
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Yang, J.; Li, Z.; Gan, X.; Zhai, G.; Gao, J.; Xiong, C.; Qiu, X.; Wang, X.; Yin, Z.; Zheng, F. Deletion of Pr130 Interrupts Cardiac Development in Zebrafish. Int. J. Mol. Sci. 2016, 17, 1746.

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