PUBLICATION

Proprotein Convertase Furina Is Required for Heart Development in Zebrafish

Authors
Zhou, Q., Lei, L., Zhang, H., Chiu, S.C., Gao, L., Yang, R., Wei, W., Peng, G., Zhu, X., Xiong, J.W.
ID
ZDB-PUB-211009-4
Date
2021
Source
Journal of Cell Science   134(21): (Journal)
Registered Authors
Peng, Gang, Xiong, Jing-Wei, Zhang, Hefei
Keywords
Cardiac trabeculation, Furina, Heart looping, Loft mutant, Zebrafish
MeSH Terms
  • Animals
  • Heart
  • Organogenesis/genetics
  • Proprotein Convertases*
  • Receptors, Notch/genetics
  • Zebrafish*/genetics
  • Zebrafish Proteins*/genetics
PubMed
34622921 Full text @ J. Cell Sci.
Abstract
Cardiac looping and trabeculation are key processes during cardiac chamber maturation. However, the underlying mechanisms remain incompletely understood. Here, we report the isolation, cloning, and characterization of the proprotein convertase furina from the cardiovascular mutant loft in zebrafish. loft is an ethylnitrosourea-induced mutant and has evident defects in the cardiac outflow tract, heart looping and trabeculation, the craniofacial region, and pharyngeal arch arteries. Positional cloning revealed that furina mRNA was barely detectable in loft mutants, and loft failed to complement the TALEN-induced furina mutant pku338, confirming that furina is responsible for the loft mutant phenotypes. Mechanistic studies demonstrated that Notch reporter Tg(tp1:mCherry) signals were largely eliminated in mutant hearts, while over-expression of NICD partially rescued the mutant phenotypes, probably due to the lack of Furina-mediated cleavage processing of Notch1b proteins, the only Notch receptor expressed in the heart. Together, our data suggest a potential post-translational modification of Notch1b proteins via the proprotein convertase Furina in the heart and unveil the function of the Furina-Notch1b axis in cardiac looping and trabeculation in zebrafish and possibly in other organisms.
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