Content area
Full text
About the Authors:
Jeffrey A. Fabrick
* E-mail: [email protected]
Affiliation: USDA-ARS, U.S. Arid Land Agricultural Research Center, Maricopa, Arizona, United States of America
Bruce E. Tabashnik
Affiliation: Department of Entomology, University of Arizona, Tucson, Arizona, United States of America
Introduction
Insecticidal crystalline proteins from the common soil bacterium Bacillus thuringiensis (Bt) kill some insect pests, but cause little or no harm to most non-target organisms including people [1]–[3]. Genetically engineered crops producing Bt proteins for insect control were first cultivated commercially in 1996 [3] and grew on more than 58 million hectares worldwide in 2010 [4]. Such Bt crops can improve yields and reduce reliance on conventional insecticides, thereby providing economic, health, and environmental benefits [5]–[8]. However, the evolution of resistance to Bt crops by insect pests can reduce such benefits.
Field-evolved resistance to Bt crops has been reported for some populations of several insect pests [9]–[15]. Although the mechanisms of resistance have not been reported for these cases, they have been identified in many laboratory-selected strains and in pest populations that evolved resistance outside of the laboratory to the Bt toxins used in sprays [2], [16]–[19]. The most common mechanism involves changes in larval midgut target sites that reduce binding of Bt toxins [20]–[25].
Here we focus on resistance to Bt toxin Cry1Ac in the pink bollworm, Pectinophora gossypiella (Saunders), one of the world's most destructive pests of cotton worldwide [26]. In western India, pink bollworm resistance to Bt cotton producing Cry1Ac is associated with widespread control failures of this crop [13]–[14]. In China, field control failures have not been reported, but pink bollworm susceptibility to Cry1Ac has decreased significantly [27]. By contrast, field populations of pink bollworm have remained susceptible to Cry1Ac in Arizona for 15 years, enabling use of Bt cotton producing either Cry1Ac alone or Cry1Ac and Cry2Ab as a primary tool of a multi-tactic eradication program [28]–[29].
Although Arizona field populations remain susceptible, several laboratory strains of pink bollworm from Arizona were selected for resistance to Cry1Ac by rearing them on diet treated with this toxin [30]–[32]. In all of these strains, including the Arizona pooled resistant strain (AZP-R), resistance to Cry1Ac and to Bt cotton producing Cry1Ac is linked with mutations in the PgCad1 gene (previously called BtR)...