4.5 Article

Neuron navigator 3 (NAV3) is required for heart development in zebrafish

期刊

FISH PHYSIOLOGY AND BIOCHEMISTRY
卷 48, 期 1, 页码 173-183

出版社

SPRINGER
DOI: 10.1007/s10695-022-01049-5

关键词

Cardiogenesis; Zebrafish; Cardiac defects; CRISPR/Cas9; In situ hybridization

资金

  1. National Natural Science Foundation of China [82000458]
  2. start-up funding for Doctoral Research of Nantong Science and Technology College [NTKY-Dr2017001]
  3. Nantong Science and Technology Program [JC2021088]
  4. Open Program of Key Laboratory of Cultivation and High-value Utilization of Marine Organisms in Fujian Province [2019fjsccq08]
  5. Natural Science Foundation of the Jiangsu Higher Education Institutions of China [20KJB180008]
  6. Science Foundation of Nantong City [JC2020023]

向作者/读者索取更多资源

The study reveals that Nav3 plays a critical role in the cardiac development of zebrafish embryos. Deletion of the nav3 gene leads to severe deficiencies in the morphology and structure of the heart in zebrafish.
As a tightly controlled biological pro- cess, cardiogenesis requires the specification and migration of a suite of cell types to form a particular three-dimensional configuration of the heart. Many genetic factors are involved in the formation and maturation of the heart, and any genetic mutations may result in severe cardiac failures. The neuron navigator (NAV) family consists of three vertebrate homologs (NAV1, NAV2, and NAV3) of the neural guidance molecule uncoordinated-53 (UNC-53) in Caenorhabditis elegans. Although they are recognized as neural regulators, their expressions are also detected in many organs, including the heart, kidney, and liver. However, the functions of NAVs, regardless of neural guidance, remain largely unexplored. In our study, we found that nav3 gene was expressed in the cardiac region of zebrafish embryos from 24 to 48 h post-fertilization (hpf) by means of in situ hybridization (ISH) assay. A CRISPR/Cas9-based genome editing method was utilized to delete the nav3 gene in zebrafish and loss of function of Nav3 resulted in a severe deficiency in its cardiac morphology and structure. The similar phenotypic defects of the knockout mutants could recur by nav3 morpholino injection and be rescued by nav3 mRNA injection. Dual-color fluorescence imaging of ventricle and atrium markers further confirmed the disruption of the heart development in nav3-deleted mutants. Although the heart rate was not affected by the deletion of nav3, the heartbeat intensity was decreased in the mutants. All these findings indicate that Nav3 was required for cardiogenesis in developing zebrafish embryos.

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