Investigation of neural developmental abnormalities in Nde1 knockout zebrafish using HuC:RFP labeling technology
10.3969/j.issn.1672-8467.2025.06.003
- VernacularTitle:利用HuC:RFP标记技术研究Nde1基因敲除斑马鱼的神经发育异常
- Author:
Ting LIU
1
;
Qi ZHANG
1
;
Jia LIN
1
;
Ying-lan ZHANG
1
;
Qiang LI
1
Author Information
1. 国家儿童医学中心/复旦大学附属儿科医院儿科研究所 上海 201102;复旦大学儿童发育与疾病转化医学中心 上海 201102;上海市出生缺陷防治重点实验室 上海 201102;国家卫生健康委员会新生儿疾病重点实验室(复旦大学)上海 201102
- Publication Type:Journal Article
- Keywords:
Nde1;
HuC:RFP;
neurodevelopment;
zebrafish
- From:
Fudan University Journal of Medical Sciences
2025;52(6):794-802
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of Nde1 gene knockout on early neural development of zebrafish by visualizing the development of neural networks in zebrafish.Methods Transgenic zebrafish Tg(Nde1-/-;HuC:RFP+/-)was constructed by crossing Nde1-/-with Tg(HuC:RFP+/-).The HuC promoter was employed to drive the expression of red fluorescent protein in neurons,which allowing the visualization of zebrafish neural networks and tracking of neural development.Furthermore,by using Image J and Prism to compare the average fluorescence intensity of neurons and the expression level of fluorescent reporter proteins between Nde1 deficiency zebrafish and wild type zebrafish,the effect of Nde1 gene knockout on zebrafish neural development was analyzed.Results From 48 hours post-fertilization(hpf)to 7 days dpf,the average fluorescence intensity of red fluorescence expressed by trigeminal sensory neurons and spinal cord neurons in Nde1 deficiency zebrafish was lower than that in wild type zebrafish.RT-qPCR results also showed that the mRNA expression level of red fluorescent reporter protein in Nde1 deficiency zebrafish was significantly lower than that in the wild type zebrafish.Conclusion Nde1 gene deletion may lead to abnormal development of trigeminal sensory neurons and spinal cordneurons by affecting neural progenitor cell differentiation and increasing apoptosis.
