PUBLICATION
Beclin 1 deficiency causes hepatic cell apoptosis via endoplasmic reticulum stress in zebrafish larvae
- Authors
- Dong, G., Zhang, Z., Duan, K., Shi, W., Huang, R., Wang, B., Luo, L., Zhang, Y., Ruan, H., Huang, H.
- ID
- ZDB-PUB-191212-34
- Date
- 2019
- Source
- FEBS letters 594(7): 1155-1165 (Journal)
- Registered Authors
- Huang, Honghui, Ruan, Hua
- Keywords
- Autophagy, Beclin 1, ER stress, cell apoptosis, protein aggregates, zebrafish
- MeSH Terms
-
- Animals
- Apoptosis*
- Autophagy
- Beclin-1/deficiency*
- Beclin-1/genetics
- Endoplasmic Reticulum Stress*
- Gene Deletion
- Genes, Essential
- Hepatocytes/cytology*
- Humans
- Larva/cytology*
- Larva/genetics
- Liver/cytology
- Liver/metabolism
- Protein Aggregates
- Zebrafish/genetics
- Zebrafish/growth & development*
- PubMed
- 31823348 Full text @ FEBS Lett.
Citation
Dong, G., Zhang, Z., Duan, K., Shi, W., Huang, R., Wang, B., Luo, L., Zhang, Y., Ruan, H., Huang, H. (2019) Beclin 1 deficiency causes hepatic cell apoptosis via endoplasmic reticulum stress in zebrafish larvae. FEBS letters. 594(7):1155-1165.
Abstract
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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping