Deletion of Pr130 Interrupts Cardiac Development in Zebrafish

Protein phosphatase 2 regulatory subunit B, alpha ( ), 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 was involved in heart failure, and PR130, the largest tr...

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Veröffentlicht in:International journal of molecular sciences 2016-11, Vol.17 (11), p.1746-1746
Hauptverfasser: Yang, Jie, Li, Zuhua, Gan, Xuedong, Zhai, Gang, Gao, Jiajia, Xiong, Chenling, Qiu, Xueping, Wang, Xuebin, Yin, Zhan, Zheng, Fang
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Sprache:eng
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Zusammenfassung:Protein phosphatase 2 regulatory subunit B, alpha ( ), 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 was involved in heart failure, and PR130, the largest transcription of , 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 -deletion zebrafish lines were generated using clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated proteins (Cas) system. -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 -knockout zebrafish compared to wild-type (WT). Taken together, our results suggest that is required for normal myocardium formation and efficient cardiac contractile function.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms17111746