Dual Oxidase Mutant Retards Mauthner-Cell Axon Regenerationat an Early Stage via Modulating Mitochondrial Dynamics in Zebrafish
Lei-Qing Yang 1• Min Chen 1• Da-Long Ren 1,2• Bing Hu 1
1 Eye Center, The First Affiliated Hospital of USTC, Hefei National Laboratory for Physical Sciences at the Microscale, Chinese Academy of Sciences Key Laboratory of Brain
Function and Disease, School of Life Sciences, Division of Biomedical Sciences, University of Science and Technology of China, Hefei 230026, China
2 Anhui Province Key Laboratory of Local Livestock and Poultry Genetic Resource Conservation and Bio-breeding, College of Animal Science and Technology, Anhui Agricultural
University, Hefei 230036, China
Abstract
Dual oxidase (duox)-derived reactive oxygen species (ROS) have been correlated with neuronal polarity, cerebellar development, and neuroplasticity. However, there have not been many comprehensive studies of the effect of individual duox isoforms on central-axon regeneration in vivo. Here, we explored this question in zebrafish, an excellent model organism for central-axon regeneration studies. In our research, mutation of the duox gene with CRISPR/Cas9 significantly retarded the single-axon regeneration of the zebrafish Mauthner cell in vivo. Using deep transcriptome sequencing, we found that the expression levels of related functional enzymes in mitochondria were down-regulated in duox mutant fish. In vivo imaging showed that duox mutants had significantly disrupted mitochondrial transport and redox state in single Mauthner-cell axon. Our research data provide insights into how duox is involved in central-axon regeneration by changing mitochondrial transport.
Keywords
duox； Zebrafish； Mauthner cell； Axon regeneration； Mitochondrial dynamics
