Bt Research 2024, Vol.15, No.5, 215-222 http://microbescipublisher.com/index.php/bt 218 Figure 1 Genome of B. thuringiensis strain GR007 (Adopted from Pacheco et al., 2021) 5 Mechanisms of Resistance to Bt 5.1 Molecular mechanisms of insect resistance Insect resistance to Bacillus thuringiensis (Bt) toxins is primarily driven by genetic mutations that alter the structure and function of midgut receptors, which are crucial for toxin binding. For instance, mutations in the ABC transporter subfamily C genes, specifically ABCC2 and ABCC3, have been linked to high levels of resistance in several lepidopteran species, including the diamondback moth, Plutella xylostella. CRISPR/Cas9-mediated knockout studies have demonstrated that these genes are essential for the binding of Cry1Ac toxins to midgut brush border membrane vesicles, thereby confirming their role as functional receptors for Bt toxins (Guo et al., 2019). Additionally, other studies have identified mutations in genes coding for surrogate receptors as significant contributors to resistance (Pinos et al., 2021). 5.2 Genomic studies on resistance evolution Genomic approaches have been instrumental in uncovering the mutations responsible for Bt resistance. Research on the European corn borer, Ostrinia nubilalis, has provided significant insights into the genetic basis of resistance. These studies have identified specific mutations that alter the binding receptor structure in the midgut, which directly impacts the efficacy of Bt toxins (Xuan, 2024). Such genomic studies are crucial for understanding the evolution of resistance and for developing strategies to mitigate it (Coates, 2016). Furthermore, comprehensive reviews of field-evolved resistance have highlighted the importance of key resistance genes in maintaining the sustainability of Bt technology.
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