Plutella xylostella (L., 1758) (Lepidoptera: Plutellidae) is a major insect pest of cruciferous crops worldwide. The most common biopesticides used to control P. xylostella are based on the entomopathogenic bacterium Bacillus thuringiensis Berliner (Bt) (Bacillaceae). P. xylostella was the first insect in which field resistance to Bt was identified. Although many different insects are susceptible to Cry toxins, the Bt mode of action is not clear cut. An elaborate model involving the sequential binding of the toxins to different membrane receptors has been proposed to describe the events leading to membrane insertion and pore formation. However, it has also been proposed that, in contradiction to mechanism, Bt toxins function by activating intracellular signaling pathways which lead to the necrotic death of their target cells without the need for pore formation. The understanding of the mechanism of action of Bt toxins has been complicated recently by the discovery that mutations in the gene encoding an ABCC2 transporter are responsible for resistance to Bt toxins in four different insect species. Laboratory studies with Spodoptera exigua (Huebner, 1808) (Lepidoptera: Noctuidae) identified a group of proteins, know as REPAT (REsponse to PAThogens) proteins were found to be up-regulated in response to not only Cry toxins, but also to B. thuringiensis and other microbial pathogens. Genomic and proteomic approaches have begun to unravel how invertebrate defenses respond to Bt toxins on a biochemical and cellular level. In general exposure to Bt results in the altered expression of many genes including the repat superfamily that are induced by a variety of pathogens. Various different functions have been subscribed to the insect genes that are differentially expressed upon exposure to Bt including immune defense, toxin activation or binding, oxidative or general metabolism and stress response. The aim of this research is to test the hypothesis that the susceptibility of P. xylostella to Bt correlates with the level of expression of components of this putative stress-response regulon. This will include investigating whether suppression of some components affects the expression of others via a feedback mechanism.
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