PUBLICATION

DUSP2 deletion with CRISPR/Cas9 promotes Mauthner cell axonal regeneration at the early stage of zebrafish

Authors
Shao, G.J., Wang, X.L., Wei, M.L., Ren, D.L., Hu, B.
ID
ZDB-PUB-220827-36
Date
2023
Source
Neural regeneration research   18: 577-581 (Journal)
Registered Authors
Hu, Bing
Keywords
CRISPR/Cas9, DUSP2, JNK, Mauthner cell, axon regeneration, central nervous system, single-cell electroporation, spinal cord injury, two-photon axotomy, zebrafish
MeSH Terms
none
PubMed
36018180 Full text @ Neural Regen Res
Abstract
Axon regeneration of central neurons is a complex process that is tightly regulated by multiple extrinsic and intrinsic factors. The expression levels of distinct genes are changed after central neural system (CNS) injury and affect axon regeneration. A previous study identified dusp2 as an upregulated gene in zebrafish with spinal cord injury. Here, we found that dual specificity phosphatase 2 (DUSP2) is a negative regulator of axon regeneration of the Mauthner cell (M-cell). DUSP2 is a phosphatase that mediates the dephosphorylation of JNK. In this study, we knocked out dusp2 by CRISPR/Cas9 and found that M-cell axons of dusp2-/- zebrafish had a better regeneration at the early stage after birth (within 8 days after birth), while those of dusp2+/- zebrafish did not. Overexpression of DUSP2 in Tg (Tol 056) zebrafish by single-cell electroporation retarded the regeneration of M-cell axons. Western blotting results showed that DUSP2 knockout slightly increased the levels of phosphorylated JNK. These findings suggest that knocking out DUSP2 promoted the regeneration of zebrafish M-cell axons, possibly through enhancing JNK phosphorylation.
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