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作 者:Guo-Jian Shao Xin-Liang Wang Mei-Li Wei Da-Long Ren Bing Hu
机构地区:[1]School of Life Sciences,Division of Biomedical Sciences,University of Science and Technology of China,Hefei,Anhui Province,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,Anhui Province,China
出 处:《Neural Regeneration Research》2023年第3期577-581,共5页中国神经再生研究(英文版)
基 金:granted by the National Natural Science Foundation of China,No.82071357;Ministry of Science and Technology of China,No.2019YFA0405600(both to BH).
摘 要: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.
关 键 词:axon regeneration central nervous system CRISPR/Cas9 DUSP2 JNK Mauthner cell single-cell electroporation spinal cord injury two-photon axotomy ZEBRAFISH
分 类 号:R741[医药卫生—神经病学与精神病学]
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