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Mitochondria and Lysosomes Participate in Vip3Aa-Induced Spodoptera frugiperda Sf9 Cell Apoptosis

Xiaoyue Hou1, Lu Han1, Baoju An1

  • 1Department of Microbiology, College of Life Sciences, Nankai University, Tianjin 300071, China.

Toxins
|February 20, 2020
PubMed

Insights

Bacillus thuringiensis Vip3Aa protein induces apoptosis in Sf9 cells by causing mitochondrial dysfunction and affecting lysosomal function. Inhibiting specific enzymes protected cells, highlighting lysosomes

Area of Science:

  • Insect toxicology
  • Cell biology
  • Molecular biology

Background:

  • Vip3Aa protein from Bacillus thuringiensis induces apoptosis in Sf9 cells.
  • The precise mechanism of Vip3Aa-induced apoptosis remains unclear.

Purpose of the Study:

  • To elucidate the mechanism of Vip3Aa-induced apoptosis in Sf9 cells.
  • To investigate the roles of mitochondria and lysosomes in Vip3Aa-induced apoptosis.

Main Methods:

  • Sf9 cells were treated with Vip3Aa.
  • Mitochondrial membrane potential, reactive oxygen species (ROS), and cytochrome c release were assessed.
  • Caspase-9 and -3 activation was measured.
  • Lysosomal acridine orange retention was evaluated.
  • Cell viability was assessed after pretreatment with cathepsin inhibitors.

Main Results:

  • Vip3Aa induced mitochondrial dysfunction, including collapse of mitochondrial membrane potential, increased ROS, and cytochrome c release.
  • Vip3Aa activated caspase-9 and -3.
  • Vip3Aa impaired lysosomal function, reducing acridine orange retention.
  • Inhibitors of cathepsin L and D enhanced cell viability and reduced apoptosis markers.

Conclusions:

  • Vip3Aa induces apoptosis in Sf9 cells primarily through mitochondrial dysfunction.
  • Lysosomes play a significant role in the apoptotic pathway triggered by Vip3Aa.
  • Targeting lysosomal enzymes may offer a strategy to mitigate Vip3Aa toxicity.
Keywords:
Sf9 cellsVip3Aaapoptosislysosomemitochondria

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