内质网
细胞生物学
斑马鱼
自噬
未折叠蛋白反应
细胞凋亡
突变体
生物
程序性细胞死亡
基因
遗传学
作者
Guoping Dong,Zhe Zhang,Kun Duan,Wenna Shi,Rui Huang,Bangjun Wang,Lingfei Luo,Yaoguang Zhang,Hua Ruan,Hai Huang
出处
期刊:FEBS Letters
[Wiley]
日期:2019-12-20
卷期号:594 (7): 1155-1165
被引量:11
标识
DOI:10.1002/1873-3468.13712
摘要
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.
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