Abstract
Transgenic crops that produce Bacillus thuringiensis (Bt) proteins for pest control are grown extensively, but insect adaptation can reduce their effectiveness. Established mode of action models assert that Bt proteins Cry1Ab and Cry1Ac are produced as inactive protoxins that require conversion to a smaller activated form to exert toxicity. However, contrary to this widely accepted paradigm, we report evidence from seven resistant strains of three major crop pests showing that Cry1Ab and Cry1Ac protoxins were generally more potent than the corresponding activated toxins. Moreover, resistance was higher to activated toxins than protoxins in eight of nine cases evaluated in this study. These data and previously reported results support a new model in which protoxins and activated toxins kill insects via different pathways. Recognizing that protoxins can be more potent than activated toxins against resistant insects may help to enhance and sustain the efficacy of transgenic Bt crops.
Highlights
Asserts that protoxins do not bind to midgut receptors and must be converted to activated toxins of approximately 65 kDa to bind to larval midgut receptors and exert toxic effects[15,16,17,18]
In vitro experiments with Pectinophora gossypiella showed that both the protoxin and activated toxin forms of Cry1Ac bind to fragments of cadherin, a key midgut receptor protein, and to brush border membrane vesicles prepared from insect midguts[19]
The classical model predicts that reduced binding of activated toxins to midgut receptors, the most common and most potent mechanism of resistance, causes similar resistance to protoxins and activated toxins[27,28]
Summary
Asserts that protoxins do not bind to midgut receptors and must be converted to activated toxins of approximately 65 kDa to bind to larval midgut receptors and exert toxic effects[15,16,17,18] Contrary to this paradigm, in vitro experiments with Pectinophora gossypiella showed that both the protoxin and activated toxin forms of Cry1Ac bind to fragments of cadherin, a key midgut receptor protein, and to brush border membrane vesicles prepared from insect midguts[19]. Based primarily on the in vitro findings summarized above, Gomez et al.[21] proposed a new model for Bt mode of action, which we refer to here as the “dual model,” where both the protoxin and activated toxin forms can kill insects, with each form exerting its toxic effect via a different pathway (Fig. 1) This contrasts with what we refer to hereafter as the “classical model” described above in which protoxins are inactive. The results show that protoxins were generally more potent than activated toxins against resistant strains, which contradicts the classical model and supports the dual model
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