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Protective function of autophagy against oxidative stress in zebrafish
Author(s) -
Imamura Shintaro,
Yabu Takeshi,
Yamashita Michiaki
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.904.1
Subject(s) - autophagy , zebrafish , oxidative stress , microbiology and biotechnology , atg5 , morpholino , chemistry , biology , paraquat , biochemistry , gene , apoptosis
Autophagy is a catabolic process by the lysosomal degradation of own components in cells. Molecular mechanisms involving in the cell damage and protective process under oxidative stress have not been characterized. To identify the autophagic pathway regulating the protective function under oxidative stress conditions in vivo, zebrafish models for macroautophagy can be used. To observe the induction of autophagy in zebrafish embryos, we generated the transgenic lines which expressed MAP1‐LC3B (LC3)‐GFP fusion protein as a marker of autophagy. When zebrafish embryos were immersed in hydrogen peroxide (0.1–1000 μM), tert‐butyl hydroperoxide (BHP, 0.1–10 μM) and methyl viologen (paraquat, 10–1000 μM), LC3 was induced. Morpholino antisense oligos for ATG5 and ATG7 were used to inhibit autophagic pathways. Oxidized proteins and DNA were induced in the 24 h embryo under oxidative stress conditions. Inhibition of the ATG5 and ATG7 functions caused developmental delay and embryonic lethal under oxidative stress conditions. Autophagy deficiency caused genomic instability under oxidative stress. Some chromosomes were broken and caused gene aneuploidy. These findings indicated that autophagy was essential to prevent the accumulation of oxidized proteins and the cells with a chromosome aberration to promote normal development.