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Beclin 1 deficiency causes hepatic cell apoptosis via endoplasmic reticulum stress in zebrafish larvae
Author(s) -
Dong Guoping,
Zhang Zhe,
Duan Kun,
Shi Wenpeng,
Huang Rui,
Wang Bangjun,
Luo Lingfei,
Zhang Yaoguang,
Ruan Hua,
Huang Honghui
Publication year - 2020
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.13712
Subject(s) - endoplasmic reticulum , microbiology and biotechnology , unfolded protein response , autophagy , zebrafish , apoptosis , mutant , biology , programmed cell death , gene , genetics
Beclin 1/Atg6 is an essential autophagy gene, and deficiency of this gene in organisms leads to impaired autophagic flux, usually with cell apoptosis; however, the causative mechanism of cell apoptosis is not clear. Here, we knocked out the beclin 1 gene in zebrafish and found that autophagic flux is disrupted in mutants. Beclin 1‐deficient zebrafish live through embryogenesis but die at larval stage. We found accumulated protein aggregates and vigorous apoptosis in mutant larvae, predominantly in the liver. The hepatic cell apoptosis in mutants results from an endoplasmic reticulum (ER) stress response; however, it is not the leading cause of mutant larval lethality. Our work proposes that ER stress induces cell apoptosis in Beclin 1‐deficient organisms.