ABC transporter mis-splicing associated with resistance to Bt toxin Cry2Ab in laboratory- and field-selected pink bollworm

Abstract

Evolution of pest resistance threatens the benefits of genetically engineered crops that produce Bacillus thuringiensis (Bt) insecticidal proteins. Strategies intended to delay pest resistance are most effective when implemented proactively. Accordingly, researchers have selected for and analyzed resistance to Bt toxins in many laboratory strains of pests before resistance evolves in the field, but the utility of this approach depends on the largely untested assumption that laboratory- and field-selected resistance to Bt toxins are similar. Here we compared the genetic basis of resistance to Bt toxin Cry2Ab, which is widely deployed in transgenic crops, between laboratory- and field-selected populations of the pink bollworm (Pectinophora gossypiella), a global pest of cotton. We discovered that resistance to Cry2Ab is associated with mutations disrupting the same ATP-binding cassette transporter gene (PgABCA2) in a laboratory-selected strain from Arizona, USA, and in field-selected populations from India. The most common mutation, loss of exon 6 caused by alternative splicing, occurred in resistant larvae from both locations. Together with previous data, the results imply that mutations in the same gene confer Bt resistance in laboratory- and field-selected strains and suggest that focusing on ABCA2 genes may help to accelerate progress in monitoring and managing resistance to Cry2Ab.

Reduced cadherin expression associated with resistance to Bt toxin Cry1Ac in pink bollworm

“…Resistance to Cry1Ac and Cry2Ab in pink bollworm is associated with alternative splicing of cadherin ( PgCad1 ) and an ABC transporter ( PgABCA2 ), respectively . However, we do not yet know what causes this alternative splicing.…”

“…Resistance to Cry1Ac and Cry2Ab in pink bollworm is associated with alternative splicing of cadherin (PgCad1) and an ABC transporter (PgABCA2), respectively. 30,39 However, we do not yet know what causes this alternative splicing. The new results reported here suggest that gene regulation as well as altered post-transcriptional mRNA splicing underlie many pink bollworm resistance phenotypes.…”

“…Here we report the first evidence of reduced expression of a receptor protein associated with resistance to a Bt toxin in the pink bollworm, Pectinophora gossypiella (Saunders), one of the world's most destructive pests of cotton . Pink bollworm is currently targeted by transgenic cotton producing either Bt toxin Cry1Ac alone in China or Cry1Ac + Cry2Ab toxins in India and elsewhere . While this invasive pest has not evolved resistance to Cry1Ac in the United States and China, widespread practical resistance to Bt cotton producing Cry1Ac and Cry1Ac + Cry2Ab has evolved rapidly in India, the world leader in cotton production.…”

“…28 Pink bollworm is currently targeted by transgenic cotton producing either Bt toxin Cry1Ac alone in China or Cry1Ac + Cry2Ab toxins in India and elsewhere. 29,30 While this invasive pest has not evolved resistance to Cry1Ac in the United States and China, 8 widespread practical resistance to Bt cotton producing Cry1Ac and Cry1Ac + Cry2Ab has evolved rapidly in India, [30][31][32][33][34] the world leader in cotton production.…”

Mutations in a novel cadherin gene associated with Bt resistance inHelicoverpa zea

“…Finally, there are inherent tradeoffs to using laboratory-selected versus field-selected populations to identify genes under selection (Ffrench-Constant, 2013). On the one hand, laboratory-selected populations can provide insights into the genetic mechanisms underlying resistance (Gahan et al, 2001), and Bt resistance mutations identified in laboratory-selected populations have been found in field-selected populations (Zhang et al, 2012; Jin et al, 2018; Mathew et al, 2018; Wang et al, in press ). On the other hand, some mutations that produce resistant phenotypes in the lab cannot be found in field-collected individuals (Zhang et al, 2012; Fabrick et al, 2014; Mathew et al, 2018).…”