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Overexpression of Wld s or Nmnat2 in mauthner cells by single‐cell electroporation delays axon degeneration in live zebrafish
Author(s) -
Feng Yan,
Yan Tingting,
Zheng Jin,
Ge Xinjian,
Mu Yu,
Zhang Yi,
Wu Dongmei,
Du Jiulin,
Zhai Qiwei
Publication year - 2010
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.22498
Subject(s) - axon , mauthner cell , zebrafish , electroporation , wallerian degeneration , microbiology and biotechnology , biology , degeneration (medical) , neuroscience , in vivo , pathology , biochemistry , medicine , genetics , fishery , fish <actinopterygii> , gene
Axon degeneration is supposed to be a therapeutic target for treating neurodegenerative diseases. Mauthner cells (M‐cells) are ideal for studying axons in vivo because of their limited numbers, large size, and long axons. In this study, we labeled M‐cells by single‐cell electroporation with plasmids expressing DsRed2 or EGFP. Injury‐induced axon degeneration in labeled M‐cell was imaged under a confocal microscope, and we found that the Mauthner axons started to degenerate about 24 hr after lesion. The Wld S protein containing full‐length Nmnat1 is well‐known for its axon‐protective function in many systems. Overexpression of Wld S in M‐cells also greatly delayed axon degeneration in live zebrafish. Nmnat2 is the only Nmnat highly expressed in brain. Here we demonstrated that overexpression of Nmnat2 in M‐cells significantly delayed axon degeneration in vivo, and disruption of the NAD synthesis activity of Nmnat2 markedly attenuated its axon‐protective function. All these data show that injury‐induced axon degeneration of M‐cell has a mechanism similar to that in mammalians and would be a valuable model for studying axon degeneration in vivo. © 2010 Wiley‐Liss, Inc.