Effects of Treatment on Expression of Detoxification Genes in Chlorantraniliprole-Resistant .

Detoxification genes are crucial to insect resistance against chemical pesticides, yet their expression may be altered by exposure to biopesticides such as spores and insecticidal proteins of (Bt). Increased enzymatic levels of selected detoxification genes, including glutathione S-transferase (GST), cytochrome P450 (CYP450), and carboxylesterase (CarE), were detected in chlorantraniliprole (CAP)-resistant strains of the diamondback moth (DBM, ) from China when compared to a reference susceptible strain. These CAP-resistant DBM strains displayed distinct expression patterns of GST 1, CYP6B7, and CarE-6 after treatment with CAP and a Bt pesticide (Bt-G033).

Proactive resistance management for sustaining the efficacy of RNA interference for pest control.

Biopesticides based on RNA interference (RNAi) took a major step forward with the first registration of a sprayable RNAi product, which targets the world's most damaging potato pest. Proactive resistance management is needed to delay the evolution of resistance by pests and sustain the efficacy of RNAi biopesticides.

Individual transmembrane domains of SfABCC2 from Spodoptera frugiperda do not serve as functional Cry1F receptors.

The fall armyworm (Spodoptera frugiperda) is a major global pest causing severe damage to various crops, especially corn. Transgenic corn producing the Cry1F pesticidal protein from the bacterium Bacillus thuringiensis (Cry1F corn) showed effectiveness in controlling this pest until S. frugiperda populations at locations in North and South America evolved practical resistance.

Diverse genetic basis of Vip3Aa resistance in five independent field-derived strains of Helicoverpa zea in the US.

Background: Practical resistance of Helicoverpa zea to Cry proteins has become widespread in the US, making Vip3Aa the only effective Bacillus thuringiensis (Bt) protein for controlling this pest. Understanding the genetic basis of Vip3Aa resistance in H. zea is essential in sustaining the long-term efficacy of Vip3Aa.