CRISPR-mediated mutations in the ABC transporter gene ABCA2 confer pink bollworm resistance to Bt toxin Cry2Ab

Fabrick, Jeffrey A.; LeRoy, Dannialle M.; Mathew, Lolita G.; Wu, Yingliang; Unnithan, Gopalan C.; Yelich, Alex J.; Carrière, Yves; Li, Xianchun; Tabashnik, Bruce E.

doi:10.1038/s41598-021-89771-7

Cited by 23 publications

(20 citation statements)

References 43 publications

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“…Many ABC transporters associated with Bt resistance have been verified. The ABCA2 gene was shown to confer resistance to Bt toxin Cry2Ab [33,34]. Zhou et al [35] indicated that ABCB1 is linked to resistance to Cry1Ac toxin in P. xylostella, and Jin et al [36] indicated that ABCB6 increases gossypol susceptibility in H. armigera.…”

Section: Discussionmentioning

confidence: 99%

Knockout of ABC Transporter ABCG4 Gene Confers Resistance to Cry1 Proteins in Ostrinia furnacalis

Gao

Lin

Wang

et al. 2022

Toxins

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Ostrinia furnacalis is an important borer on maize. Long-term and large-scale planting of transgenic corn has led O. furnacalis evolving resistance and reducing the control effect. Recently, high levels of resistance to Bt Cry1 toxins have been reported to be genetically linked to the mutation or down-regulation of ABC transporter subfamily G gene ABCG4 in O. furnacalis. In order to further determine the relationship between ABCG4 gene and the resistance to Cry1 toxins in O. furnacalis, the novel CRISPR/Cas9 genome engineering system was utilized to successfully construct ABCG4-KO knockout homozygous strain. Bioassay results indicated that an ABCG4-KO strain had a higher resistance to Cry1 proteins compared with a susceptible strain (ACB-BtS). The result indicates that the ABCG4 gene may act as a receptor of the Bt Cry1 toxin in O. furnacalis. Furthermore, the development time was significantly changed in the early stage ABCG4-KO larvae, and the population parameters were also significantly changed. In summary, our CRISPR/Cas9-mediated genome editing study presents evidence that ABCG4 gene is a functional receptor for Bt Cry1 toxins, laying the foundation for further clarification of the Bt resistance mechanism.

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Section: Discussionmentioning

confidence: 99%

Knockout of ABC Transporter ABCG4 Gene Confers Resistance to Cry1 Proteins in Ostrinia furnacalis

Gao

Lin

Wang

et al. 2022

Toxins

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“…Nonetheless, we do not know the normal function of the kinesin-12 protein and cannot infer that the C546T mutation causes resistance. In future work, we aim to test the hypothesis that the C546T mutation contributes to resistance by determining if resistance is reduced when we use CRISPR/Cas9 to replace the mutant sequence in GA-R with the wild type sequence from LAB-S (Jin et al 2018; Fabrick et al 2021). If disruption of the kinesin-12 gene is not sufficient for resistance, as the results here imply, we expect that knocking out this gene would not cause resistance in a susceptible strain.…”

Section: Discussionmentioning

confidence: 99%

Novel genetic basis of resistance to Bt toxin Cry1Ac inHelicoverpa zea

Benowitz

Allan

Degain

et al. 2021

Preprint

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Crops genetically engineered to produce insecticidal proteins from the bacterium Bacillus thuringiensis (Bt) have advanced pest management, but their benefits are diminished when pests evolve resistance. Elucidating the genetic basis of pest resistance to Bt toxins can improve resistance monitoring, resistance management, and design of new insecticides. Here, we investigated the genetic basis of resistance to Bt toxin Cry1Ac in the lepidopteran Helicoverpa zea, one of the most damaging crop pests in the United States. To facilitate this research, we built the first chromosome-level genome assembly for this species. Using a genome-wide association study, fine-scale mapping, and RNA-seq, we identified a 250kb QTL on chromosome 13 that was strongly associated with resistance in a strain of H. zea that had been selected for resistance in the field and lab. This QTL contains no genes with a previously reported role in resistance or susceptibility to Bt toxins. However, within this QTL, we discovered a premature stop codon in a kinesin gene. We hypothesize that this mutation contributes to resistance. The results indicate the mutation on chromosome 13 was necessary but not sufficient for resistance, and therefore conclude that mutations in more than one gene contributed to resistance. Moreover, we found no changes in gene sequence or expression consistently associated with resistance for 11 genes previously implicated in lepidopteran resistance to Cry1Ac. Thus, the results reveal a novel and polygenic basis of resistance and extend the list of genes contributing to pest resistance to Bt toxins.

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“…41,42 The resistance to Cry2Ab in AZP-R2 originated in Bt4-R2 and is associated with mutations that disrupt a midgut ABCA2 protein that is a putative receptor for Cry2Ab in Lepidoptera. [43][44][45][46][47]…”

Section: Field Populations and Laboratory Strains Of Pink Bollwormmentioning

confidence: 99%

Responses to Bt toxin Vip3Aa by pink bollworm larvae resistant or susceptible to Cry toxins

Tabashnik

Unnithan

Yelich

et al. 2022

Pest Management Science

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BACKGROUND: Transgenic crops that make insecticidal proteins from Bacillus thuringiensis (Bt) have revolutionized management of some pests. However, evolution of resistance to Bt toxins by pests diminishes the efficacy of Bt crops. Resistance to crystalline (Cry) Bt toxins has spurred adoption of crops genetically engineered to produce the Bt vegetative insecticidal protein Vip3Aa. Here we used laboratory diet bioassays to evaluate responses to Vip3Aa by pink bollworm (Pectinophora gossypiella), one of the world's most damaging pests of cotton.RESULTS: Against pink bollworm larvae susceptible to Cry toxins, Vip3Aa was less potent than Cry1Ac or Cry2Ab. Conversely, Vip3Aa was more potent than Cry1Ac or Cry2Ab against laboratory strains highly resistant to those Cry toxins. Five Crysusceptible field populations were less susceptible to Vip3Aa than a Cry-susceptible laboratory strain (APHIS-S). Relative to APHIS-S, significant resistance to Vip3Aa did not occur in strains selected in the laboratory for > 700-fold resistance to Cry1Ac or both Cry1Ac and Cry2Ab.CONCLUSIONS: Resistance to Cry1Ac and Cry2Ab did not cause strong cross-resistance to Vip3Aa in pink bollworm, which is consistent with predictions based on the lack of shared midgut receptors between these toxins and previous results from other lepidopterans. Comparison of the Bt toxin concentration in plants relative to the median lethal concentration (LC 50 ) from bioassays may be useful for estimating efficacy. The moderate potency of Vip3Aa against Cry1Ac-and Cry2Ab-resistant and susceptible pink bollworm larvae suggests that Bt cotton producing this toxin together with novel Cry toxins might be useful as one component of integrated pest management.

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CRISPR-mediated mutations in the ABC transporter gene ABCA2 confer pink bollworm resistance to Bt toxin Cry2Ab

Cited by 23 publications

References 43 publications

Knockout of ABC Transporter ABCG4 Gene Confers Resistance to Cry1 Proteins in Ostrinia furnacalis

Knockout of ABC Transporter ABCG4 Gene Confers Resistance to Cry1 Proteins in Ostrinia furnacalis

Novel genetic basis of resistance to Bt toxin Cry1Ac inHelicoverpa zea

Responses to Bt toxin Vip3Aa by pink bollworm larvae resistant or susceptible to Cry toxins

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