4.7 Article

Genetic basis of resistance to the Vip3Aa Bt protein in Helicoverpa zea

Journal

PEST MANAGEMENT SCIENCE
Volume 77, Issue 3, Pages 1530-1535

Publisher

JOHN WILEY & SONS LTD
DOI: 10.1002/ps.6176

Keywords

Bacillus thuringiensis; Helicoverpa zea; inheritance; Vip3Aa; resistance; genetic

Funding

  1. Biotechnology Risk Assessment award from the USDA National Institute of Food and Agriculture [2020-33522-32318, 2003504]

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The study revealed that resistance to Vip3Aa in H. zea is monogenic, autosomal, and recessive, with no maternal effects or sex linkage observed. Resistance is largely determined by a single gene, providing valuable insights for understanding the resistance mechanism and developing effective resistance management strategies.
BACKGROUND Helicoverpa zea is a destructive pest and target of maize and cotton expressing Cry and Vip3Aa proteins in North America. The efficacy of Cry proteins against H. zea in the USA has been largely compromised by resistance. A rapid shift towards planting Bt cotton and maize producing Vip3Aa will accelerate evolution of resistance to Vip3Aa in H. zea. Research on the genetic basis of Vip3Aa resistance in H. zea is urgently needed, and can provide fundamental information for managing resistance in this pest. Here, we characterize the inheritance of Vip3Aa resistance in H. zea. RESULTS Susceptibility of a Vip3Aa-susceptible strain (SS), a resistant strain (RR), and progeny from different crosses against Vip3Aa39 was determined. RR was established from an F-2 screening of a population from Texas sampled in 2019. RR had a resistance ratio of 45194.1-fold against Vip3Aa39 relative to SS. Maternal effects and sex linkage were absent in RR. The dominance D value, calculated based on median lethal concentration (LC50) values, was -1.0 and the effective dominance (D-ML), calculated based on a given Vip3Aa39 concentration, was <= 0.0 at concentrations of 0.1-31.6 mu g cm(-2). The test using a monogenic mode of inheritance showed that resistance to Vip3Aa in H. zea was largely due to a single gene. CONCLUSION Results of this study indicate that Vip3Aa resistance in H. zea is monogenic, autosomal, and recessive. This information is valuable for studying the mechanism of Vip3Aa resistance, monitoring of resistance development, and designing appropriate strategies for preventive management of Vip3Aa resistance.

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