Dual Oxidase Mutant Retards Mauthner-Cell Axon Regeneration at an Early Stage via Modulating Mitochondrial Dynamics in Zebrafish

Yang, Lei-qing; Chen, Min; Ren, Da-long; Hu, Bing

doi:10.1007/s12264-020-00600-9

Cited by 11 publications

(8 citation statements)

References 49 publications

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“…Previous studies have shown the M-cells’ ability for regeneration [ 32 – 34 ]. The transgenic line Tg (Tol 056: EGFP) was mated with the wfs1b mutant line and the Tg (Tol 056: EGFP)/ wfs1b −/− zebrafish line was obtained so as to explore what role wfs1b plays in M-cell axon regeneration (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…The M-cell is a single pair of motor neurons in the brain stem of zebrafish which regulates the escape response triggered by abrupt stimuli [ 28 , 29 ]. According to recent studies, M-cells show a strong ability to regenerate in zebrafish in contrast to the inability to regenerate in the adult mammalian CNS [ 30 – 34 ], allowing zebrafish to become an emerging model to investigate spinal-cord injury (SCI), which remains a major cause of morbidity and societal expense on account of its global prevalence [ 35 , 36 ]. SCI and degenerative CNS disorders may cause axon degeneration, which is regarded as a therapeutic target for treating neurodegenerative diseases [ 37 , 38 ].…”

Section: Introductionmentioning

confidence: 99%

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Wolfram syndrome 1b mutation suppresses Mauthner-cell axon regeneration via ER stress signal pathway

Wang

Shi

et al. 2022

acta neuropathol commun

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Wolfram Syndrome (WS) is a fatal human inherited disease with symptoms of diabetes, vision decreasing, and neurodegeneration caused by mutations in the endoplasmic reticulum (ER)-resident protein WFS1. WFS1 has been reported to play an important role in glucose metabolism. However, the role of WFS1 in axonal regeneration in the central nervous system has so far remained elusive. Herein, we established a model of the wfs1b globally deficient zebrafish line. wfs1b deficiency severely impeded the Mauthner-cell (M-cell) axon regeneration, which was partly dependent on the ER stress response. The administration of ER stress inhibitor 4-Phenylbutyric acid (4-PBA) promoted M-cell axon regeneration in wfs1b−/− zebrafish larvae, while the ER stress activator Tunicamycin (TM) inhibited M-cell axon regeneration in wfs1b+/+ zebrafish larvae. Moreover, complementation of wfs1b at the single-cell level stimulated M-cell axon regeneration in the wfs1b−/− zebrafish larvae. Altogether, our results revealed that wfs1b promotes M-cell axon regeneration through the ER stress signal pathway and provide new evidence for a therapeutic target for WS and axon degeneration.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Wolfram syndrome 1b mutation suppresses Mauthner-cell axon regeneration via ER stress signal pathway

Wang

Shi

et al. 2022

acta neuropathol commun

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“…Accordingly, studies utilizing CRISPR/Cas9 in zebrafish have rapidly increased. In particular, studies to elucidate the role of mitochondria in neutrophil motility 70 , tRNA biogenesis and the physiology of cardiomyocytes 71 , 72 , neuronal regeneration 73 , neurodegeneration in Parkinson’s disease 74 , 75 and cellular metabolism regulation of mitochondrial abundance 76 , 77 have been reported. Furthermore, studies illustrating the role of the endoplasmic (sarcoplasmic) reticulum included REEP5 -gene knockout, which was used to elucidate the previously unknown regulation of ER/SR membrane protein organization and stress response in cardiac myocytes 78 .…”

Section: Biomedical Research Iv: Metabolic Disordersmentioning

confidence: 99%

Zebrafish as an animal model for biomedical research

et al. 2021

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Zebrafish have several advantages compared to other vertebrate models used in modeling human diseases, particularly for large-scale genetic mutant and therapeutic compound screenings, and other biomedical research applications. With the impactful developments of CRISPR and next-generation sequencing technology, disease modeling in zebrafish is accelerating the understanding of the molecular mechanisms of human genetic diseases. These efforts are fundamental for the future of precision medicine because they provide new diagnostic and therapeutic solutions. This review focuses on zebrafish disease models for biomedical research, mainly in developmental disorders, mental disorders, and metabolic diseases.

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“…Regrowth occurs following injuries between 10% and 50% of the total axon length but is very poor when axotomy is located both close as well as distant to the soma [34]. Regeneration capacity of the Mauthner axon could be enhanced by increasing cyclic adenosine monophosphate (cAMP) levels and mitochondrial transport [36,122], highlighting cellular energetics as a strategy to promote axonal regrowth and functional recovery after SCI [123,124]. The initiation of sprouting, as well as the selection of the optimal trajectory to establish functional synapses, is of crucial importance for successful pathfinding and functional axon regeneration.…”

Section: Intrinsic Regenerative Capacitymentioning

confidence: 99%

Know How to Regrow—Axon Regeneration in the Zebrafish Spinal Cord

Tsata

Wehner

2021

Cells

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The capacity for long-distance axon regeneration and functional recovery after spinal cord injury is poor in mammals but remarkable in some vertebrates, including fish and salamanders. The cellular and molecular basis of this interspecies difference is beginning to emerge. This includes the identification of target cells that react to the injury and the cues directing their pro-regenerative responses. Among existing models of successful spinal cord regeneration, the zebrafish is arguably the most understood at a mechanistic level to date. Here, we review the spinal cord injury paradigms used in zebrafish, and summarize the breadth of neuron-intrinsic and -extrinsic factors that have been identified to play pivotal roles in the ability of zebrafish to regenerate central nervous system axons and recover function.

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Dual Oxidase Mutant Retards Mauthner-Cell Axon Regeneration at an Early Stage via Modulating Mitochondrial Dynamics in Zebrafish

Cited by 11 publications

References 49 publications

Wolfram syndrome 1b mutation suppresses Mauthner-cell axon regeneration via ER stress signal pathway

Wolfram syndrome 1b mutation suppresses Mauthner-cell axon regeneration via ER stress signal pathway

Zebrafish as an animal model for biomedical research

Know How to Regrow—Axon Regeneration in the Zebrafish Spinal Cord

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