article · Toxins
Insecticidal proteins produced by Bacillus thuringiensis face operational challenges due to evolving resistance in target pests. This research investigates the molecular mechanisms of resistance to the Cry1Ac toxin in the diamondback moth, Plutella xylostella. The full-length sequence of a novel midgut trypsin gene, PxTryp_SPc1, was cloned and shown to be predominantly expressed in the midgut across all larval stages. In a resistant laboratory strain, reduced expression of PxTryp_SPc1 led to lower trypsin protease activity, which hindered Cry1Ac protoxin activation and conferred higher resistance to the protoxin than to the pre-activated toxin. This reduced expression was genetically linked to Cry1Ac resistance and decreased further under high protoxin selection pressure. Silencing PxTryp_SPc1 via RNA interference in susceptible larvae also decreased sensitivity to the protoxin, confirming the role of midgut proteases in resistance mechanisms.
Diamondback moths cause substantial damage to crops, and their ability to evolve resistance threatens the effectiveness of Bacillus thuringiensis biopesticides. Identifying the genetic and biochemical basis of this resistance, specifically how altered midgut protease activity prevents toxin activation, helps researchers understand resistance pathways and aids the broader development of more durable pest management strategies.
This work represents early-stage, laboratory-based discovery research into insect resistance mechanisms. While the abstract does not describe an immediate commercial product or applied pathway, the identification of PxTryp_SPc1 provides molecular insights that could assist developers of pest control solutions in designing resistance monitoring assays or formulating toxins that do not rely on standard midgut activation. Any commercial application remains far from real-world deployment.
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Bacillus thuringiensis (Bt) produce diverse insecticidal proteins to kill insect pests. Nevertheless, evolution of resistance to Bt toxins hampers the sustainable use of this technology. Previously, we identified down-regulation of a trypsin-like serine protease gene PxTryp_SPc1 in the midgut transcriptome and RNA-Seq data of a laboratory-selected Cry1Ac-resistant Plutella xylostella strain, SZ-R. We show here that reduced PxTryp_SPc1 expression significantly reduced caseinolytic and trypsin protease activities affecting Cry1Ac protoxin activation, thereby conferring higher resistance to Cry1Ac protoxin than activated toxin in SZ-R strain. Herein, the full-length cDNA sequence of PxTryp_SPc1 gene was cloned, and we found that it was mainly expressed in midgut tissue in all larval instars. Subsequently, we confirmed that the PxTryp_SPc1 gene was significantly decreased in SZ-R larval midgut and was further reduced when selected with high dose of Cry1Ac protoxin. Moreover, down-regulation of the PxTryp_SPc1 gene was genetically linked to resistance to Cry1Ac in the SZ-R strain. Finally, RNAi-mediated silencing of PxTryp_SPc1 gene expression decreased larval susceptibility to Cry1Ac protoxin in the susceptible DBM1Ac-S strain, supporting that low expression of PxTryp_SPc1 gene is involved in Cry1Ac resistance in P. xylostella. These findings contribute to understanding the role of midgut proteases in the mechanisms underlying insect resistance to Bt toxins.
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DOI: 10.3390/toxins12020076
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