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ARS Home » Pacific West Area » Maricopa, Arizona » U.S. Arid Land Agricultural Research Center » Pest Management and Biocontrol Research » Research » Publications at this Location » Publication #389559

Research Project: Sustainable Pest Management for Arid-Land Agroecosystems

Location: Pest Management and Biocontrol Research

Title: Novel genetic basis of resistance to Bt toxin Cry1Ac in Helicoverpa zea

item BENOWITZ, KYLE - University Of Arizona
item ALLAN, CARSON - University Of Arizona
item DEGAIN, BENJAMIN - University Of Arizona
item LI, XIANCHUN - University Of Arizona
item Fabrick, Jeffrey
item TABASHNIK, BRUCE - University Of Arizona
item CARRIERE, YVES - University Of Arizona
item MATZKIN, LUCIANO - University Of Arizona

Submitted to: Genetics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/25/2022
Publication Date: 3/23/2022
Citation: Benowitz, K.M., Allan, C.W., Degain, B.A., Li, X., Fabrick, J.A., Tabashnik, B.E., Carriere, Y., Matzkin, L.M. 2022. Novel genetic basis of resistance to Bt toxin Cry1Ac in Helicoverpa zea. Genetics. 221(1). Article iyac037.

Interpretive Summary: Crops genetically altered to produce insecticidal proteins from Bacillus thuringiensis (Bt) are grown globally and are critical for managing many insect pests. However, pest resistance to Bt crops reduces their benefits and represents a critical threat to this technology. Understanding the genetic basis of such resistance is needed to better monitor, manage, and counter pest resistance to Bt crops. Here, an ARS scientist at Maricopa, AZ and collaborators used several genomic approaches to investigate the genetic basis of resistance to the Bt toxin Cry1Ac in the key U.S. agricultural pest Helicoverpa zea. The team first assembled a chromosome-level genome using the Cry1Ac-resistant H. zea strain, GA-R. The Cry1Ac resistance genotype was mapped within a 250 kb region located on chromosome 13, which contained no genes previously identified as being involved in Bt resistance or susceptibility to Bt toxins. Additional RNA sequencing further demonstrated that this region of chromosome 13 does not control the expression of any such previously predicted genes, confirming the hypothesis that Cry1Ac resistance in GA-R derives from a novel mechanism. Comprehensive scanning for gene mutations located within this genetic locus revealed that a single base mutation in a putative kinesin gene may partially contribute to the effect of chromosome 13 on resistance in GA-R. This study supports the previous findings that the genetic basis of resistance to Cry1Ac in H. zea is controlled by several genes. The identification of such genes involved in resistance to Bt crops is essential for resistance monitoring to Bt transgenic crops and for making improved decisions for management of resistance in the field.

Technical Abstract: 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, which has 31 chromosomes containing 375'Mb and 15,482 predicted proteins. Using a genome-wide association study, fine-scale mapping, and RNA-seq, we identified a 250-kb quantitative trait locus (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. The mutation in this QTL contributed to but was not sufficient for resistance, which implies alleles in more than one gene contributed to resistance. This QTL contains no genes with a previously reported role in resistance or susceptibility to Bt toxins. However, in resistant insects, this QTL has a premature stop codon in a kinesin gene which is a primary candidate as a mutation contributing to resistance. 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.