Bacillus thuringiensis Vip3Aa Toxin Resistance in Heliothis virescens (Lepidoptera: Noctuidae)

Abstract

Laboratory selection with Vip3Aa of a field-derived population of Heliothis virescens produced Ͼ2,040-fold resistance in 12 generations of selection. The Vip3Aa-selected (Vip-Sel)-resistant population showed little cross-resistance to Cry1Ab and no cross-resistance to Cry1Ac. Resistance was unstable after 15 generations without exposure to the toxin. F 1 reciprocal crosses between Vip3Aa-unselected (Vip-Unsel) and Vip-Sel insects indicated a strong paternal influence on the inheritance of resistance. Resistance ranged from almost completely recessive (mean degree of dominance [h] ϭ 0.04 if the resistant parent was female) to incompletely dominant (mean h ϭ 0.53 if the resistant parent was male). Results from bioassays on the offspring from backcrosses of the F 1 progeny with Vip-Sel insects indicated that resistance was due to more than one locus. The results described in this article provide useful information for the insecticide resistance management strategies designed to overcome the evolution of resistance to Vip3Aa in insect pests.IMPORTANCE Heliothis virescens is an important pest that has the ability to feed on many plant species. The extensive use of Bacillus thuringiensis (Bt) crops or spray has already led to the evolution of insect resistance in the field for some species of Lepidoptera and Coleoptera. The development of resistance in insect pests is the main threat to Bt crops. The effective resistance management strategies are very important to prolong the life of Bt plants. Lab selection is the key step to test the assumption and predictions of management strategies prior to field evaluation. Resistant insects offer useful information to determine the inheritance of resistance and the frequency of resistance alleles and to study the mechanism of resistance to insecticides.

Cross‐resistance to purified Bt proteins, Bt corn and Bt cotton in a Cry2Ab2‐corn resistant strain of Spodoptera frugiperda

“…43 The symmetrical pattern with no cross-resistance is most common because Bt proteins from different classes generally lack shared binding sites, 32 and it has been documented between Cry1 and Cry2 in T. ni 38,44 and D. saccharalis (Huang et al, unpublished data) 45 and Cry1 and Vip3A in H. virescens. 46,47 The other two patterns of cross-resistance are not expected for the same reason; the Bt proteins from different classes have different modes of action and different binding sites. The symmetrical pattern with cross-resistance has never been reported in any study.…”

Bacillus thuringiensis vegetative insecticidal protein family Vip3A and mode of action against pest Lepidoptera

“…This resistant strain also showed weak cross resistance to Cry1Ab, but no cross resistance to Cry1Ac. The resistance of this strain to Vip3Aa remained unstable after rearing for several generations without Vip3Aa toxin selection . The expression of Vip3A toxin and Cry toxin in the same plant not only increased insecticidal activity against target insects but also reduced the chance of cross resistance …”

HT‐SuperSAGE of the gut tissue of a Vip3Aa‐resistant Heliothis virescens (Lepidoptera: Noctuidae) strain provides insights into the basis of resistance

“…The process of obtaining the H. virescens Vip-Sel and Vip-Unsel subpopulations, resistant and susceptible to the Vip3Aa protoxin respectively, was previously described (Pickett, 2009;Gulzar et al, 2012;Pickett et al, 2017). Briefly, a field-derived population of H. virescens (WF06) was divided into two subpopulations at the larval stage of the second generation of laboratory culture.…”

“…In our laboratory, 12 generations of selection with Vip3Aa of a field-derived population of Heliothis virescens produced a strain (Vip-Sel) with more than 2040 fold resistance compared to the genetically similar unselected (Vip-Unsel) subpopulation (Pickett, 2009;Pickett et al, 2017). Genetic characterization of Vip3Aa resistance in Vip-Sel combined with bioassays indicated resistance was due to more than one locus and appeared to be relatively unstable after 13 generations without exposure to the toxin.…”

“…Genetic characterization of Vip3Aa resistance in Vip-Sel combined with bioassays indicated resistance was due to more than one locus and appeared to be relatively unstable after 13 generations without exposure to the toxin. Inheritance of resistance showed strong paternal influence and ranged from almost completely recessive (mean h = 0.04 if the resistant parental was female) to incompletely dominant (mean h = 0.53 if the resistant parental was male) (Pickett, 2009;Pickett et al, 2017). Further characterization of the Vip-Sel subpopulation revealed a temperature-dependent fitness cost associated with reduced mating success, fecundity, and fertility in resistant insects (Gulzar et al, 2012).…”