|Tabashnik, Bruce -|
Submitted to: PLoS One
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: April 18, 2012
Publication Date: April 18, 2012
Citation: Fabrick, J.A., Tabashnik, B.E. 2012. Similar genetic basis of resistance to bt toxin cry1ac in boll-selected and diet-selected strains of pink bollworm. PLoS One. 7(4):e35658 Interpretive Summary: Much of the cotton currently grown in the U.S. has been genetically engineered to produce insecticidal proteins from the bacterium, Bacillus thuringiensis or Bt. These Bt proteins target major agricultural pests, including the pink bollworm, Pectinophora gossypiella. The pink bollworm is a major cotton pest shown to become resistant to Bt proteins in the laboratory and to Bt cotton in the field. In previous studies, resistant strains of pink bollworm were selected on artificial diet containing the Bt protein and changes or mutations in a gene called cadherin were linked with resistance to Bt. Here, we show that a novel cadherin mutation is responsible for resistance to the Bt protein and Bt cotton in a strain of pink bollworm selected on Bt cotton in the laboratory. These results reveal new information regarding the underlying genetic mechanism of Bt resistance and provides a new marker for detection of field-evolved resistance to Bt crops.
Technical Abstract: Genetically engineered cotton and corn plants producing insecticidal Bacillus thuringiensis (Bt) toxins kill some key insect pests. Yet, evolution of resistance by pests threatens long-term insect control by these transgenic Bt crops. We compared the genetic basis of resistance to Bt toxin Cry1Ac in two independently derived, laboratory-selected strains of a major cotton pest, the pink bollworm (Pectinophora gossypiella [Saunders]). The Arizona pooled resistant strain (AZP-R) was started with pink bollworm from 10 field populations and selected with Cry1Ac in diet. The Bt4R resistant strain was started with a long-term susceptible laboratory strain and selected first with Bt cotton bolls and later with Cry1Ac in diet. Previous work showed that AZP-R had three recessive mutations (r1, r2, and r3) in the pink bollworm cadherin gene (PgCad1) linked with resistance to Cry1Ac and Bt cotton. Here we report that inheritance of resistance to a diagnostic concentration of Cry1Ac was recessive in Bt4R. In interstrain complementation tests for allelism, F1 progeny from crosses between AZP-R and Bt4R were resistant to Cry1Ac, indicating a shared resistance locus in the two strains. Molecular analysis of the Bt4R cadherin gene identified a novel 15-bp deletion (r4) predicted to cause the loss of five amino acids upstream of the toxin-binding region of the cadherin protein. Four recessive mutations in PgCad1 are now implicated in resistance in five independent strains, showing that mutations in cadherin are the primary mechanism of resistance to Cry1Ac in laboratory-selected strains of pink bollworm from Arizona.