Retrotransposon-mediated disruption of a chitin synthase gene confers insect resistance to Bacillus thuringiensis Vip3Aa toxin



The development of resistance to insecticides is a major threat to global food security, with many insect pests becoming increasingly resistant to the widely used Bt toxins, including Vip3Aa, produced by the bacterium Bacillus thuringiensis. Previously, the discovery of a novel mechanism of resistance to Bt toxins has shed new light on the intricate dynamics between insects and their pathogens. A recent study published in the journal Nature has revealed that a specific retrotransposon-mediated disruption of a chitin synthase gene in the insect genome is responsible for conferring resistance to Bt Vip3Aa toxin.


Bt toxins, such as Vip3Aa, are a class of insecticidal proteins that target specific receptors in the insect midgut, causing cessation of feeding and ultimately leading to insect death. The widespread use of Bt toxins as a biopesticide has led to the development of resistance in many insect pests, posing significant challenges to integrated pest management strategies.


To investigate the genetic basis of resistance to Bt Vip3Aa toxin, researchers conducted a combination of functional genomics, transcriptomics, and biochemical analyses. They identified a specific chitin synthase gene, Chitin synthesis gene 1 (Chit1), which was disrupted by a retrotransposon insertion in the genome of the insect pest, Spodoptera exigua. The authors used CRISPR-Cas9 gene editing to recreate the disrupted Chit1 gene in a susceptible insect strain and evaluated its susceptibility to Bt Vip3Aa toxin.


The study found that the disruption of the Chit1 gene in the insect genome led to a significant reduction in the expression of chitin synthase, an enzyme responsible for the synthesis of chitin, a critical component of the insect exoskeleton. The absence of chitin synthesis led to an increased susceptibility to Bt Vip3Aa toxin, as the insect’s midgut was no longer able to anchor the toxin, allowing it to be transported out of the insect and neutralized. Conversely, the intact Chit1 gene in the resistant insect strain was found to be highly expressed, leading to the formation of a chitin-based matrix that effectively protected the insect from the toxic effects of Bt Vip3Aa.


This study highlights the importance of retrotransposon-mediated disruption of genes involved in insect development and physiology, such as chitin synthesis, in conferring resistance to Bt Vip3Aa toxin. The findings have significant implications for the development of novel strategies for managing insect resistance to Bt toxins and may lead to the development of new insecticides or biocontrol agents. Furthermore, the study demonstrates the power of functional genomics and CRISPR-Cas9 gene editing in elucidating the complex mechanisms underlying insect resistance to Bt toxins.


 Wang et al. (2022). Retrotransposon-mediated disruption of a chitin synthase gene confers insect resistance to Bacillus thuringiensis Vip3Aa toxin. Nature, 609, 104-109.


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