4.7 Article

Bacillus thuringiensis cry toxin triggers autophagy activity that may enhance cell death

Journal

PESTICIDE BIOCHEMISTRY AND PHYSIOLOGY
Volume 171, Issue -, Pages -

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.pestbp.2020.104728

Keywords

Autophagy; Bacillus thuringiensis; Pore-forming toxin; AMPK; JNK

Funding

  1. National Nature Science foundation of China [31372260]
  2. PAPPIT Direction general de asuntos del personal academico UNAM, Mexico [IN203619]
  3. Fundamental Research Funds for the Central Universities of Central China Normal University [CCNU19QN009]

Ask authors/readers for more resources

The study found that Cry toxins induce autophagy only in susceptible cell lines, depending on AMPK and JNK pathways. Inhibiting autophagy delays cell death triggered by Cry toxins.
Although it is well known that Bacillus thuringiensis Cry toxins kill insect pest by disrupting midgut cells of susceptible larvae through their pore formation activity, it is not clear what intracellular events are triggered after pore formation on the cell membrane of the target cells. Here we analyzed the role of Cry toxins on autophagy activation using several cell lines as models as well as in Helicoverpa armigera larvae. The selected insect cell lines (Hi5, Sl-HP and Sf9) were susceptible to activated Cry1Ca toxin, but only Sl-HP cells were also susceptible to activated Cry1Ac toxin. In contrast, the mammalian cell line 293 T was not susceptible to Cry1Ac or to Cry1Ca. Results show that Cry toxins induced autophagy only in the susceptible cell lines as shown by the analysis of the changes in the ratio of Atg8-PE to Atg8 and by formation of autophagosome dots containing Atg8-PE. The Cry1Ac enhanced autophagy in the midgut tissue of H. armigera larvae. Silencing expression of specific genes by RNAi assays confirmed that the autophagy induced by activated Cry toxins was dependent on AMPK and JNK pathways. Finally, inhibition of autophagy in the cell lines by specific inhibitors or RNAi assays resulted in delayed cell death triggered by Cry toxins, suggesting that the increased autophagy activity observed after toxin intoxication may contribute to cell death.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.7
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available