ZFIN ID: ZDB-PUB-191212-34
Beclin 1 deficiency causes hepatic cell apoptosis via endoplasmic reticulum stress in zebrafish larvae
Dong, G., Zhang, Z., Duan, K., Shi, W., Huang, R., Wang, B., Luo, L., Zhang, Y., Ruan, H., Huang, H.
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.
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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.
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