Learning the ABCs of Bt: ABC transporters and insect resistance to Bacillus thuringiensis provide clues to a crucial step in toxin mode of action

Insecticidal crystal toxins from the bacterium Bacillus thuringiensis (Bt) kill insects via a complex mode of action resulting in the creation of cytolytic pores in the membrane of midgut epithelial cells. Recent genetic studies in four species of Lepidoptera have found mutations in an ABC transporter in strains that have evolved resistance to Cry1A toxins. This points to a novel role of ABC proteins in insertion of pores into the membrane, and suggests strategies to increase efficacy of and delay resistance to Bt toxins.

Graphical abstractFigure optionsDownload full-size imageDownload as PowerPoint slideHighlights► Positional cloning has identified a novel resistance mechanism to Bacillus thuringiensis (Bt) toxins. ► Resistance is due to a variety of mutations in the same ABC transporter, ABCC2. ► ABCC2 is correlated with high-affinity Cry1A toxin binding to the midgut epithelium. ► The ATP-driven transport cycle facilitates toxin insertion into the membrane. ► Manipulating this cycle may increase potency of Bt toxins and delay resistance.