Monitoring for resistance to transgenic cotton

Abstract

In the 2004/05 season Bollgard II® replaced Ingard® as the transgenic variety of cotton available to Australian growers. It improves on Ingard® by incorporating an additional insecticide protein (Cry2Ab) to combat H. armigera. Sequence information indicates that these genes are distantly related and the toxins they encode do not share a common binding site. Consequently it is thought unlikely that a single mechanism could confer resistance to both toxins. Due to the perceived difficulty for H. armigera to evolve resistance to both proteins within Bollgard II®, the RMP for transgenic cotton was relaxed to allow growers to plant up to around 95% of the total area to this product. Bollgard II® was well adopted, with >70% planted area throughout the industry.

The cotton industry has sought to acquire early warnings of changes in sensitivity of insect populations to toxins that may signal the presence of resistance to transgenic varieties of cotton. The sensitivity of field-collected populations of H. armigera and H. punctigera to Bt products was assayed before and subsequent to the widespread deployment of Ingard® cotton expressing Cry1Ac in the mid-1990’s. During CSE102C, baseline levels of susceptibility to Cry2Ab were established in preparation for replacement in the 2004/05 season of Ingard® with Bollgard II®.

Preserving the efficacy of Cry1Ac and Cry2Ab is critical for the future of the industry, not only for the efficacy of the Bollgard II® varieties of cotton, but also for the long-term future of cotton varieties expressing Cry1Ac or Cry2Ab in combination with other effective toxins.

In this project we achieved our main aim of rigorously assessing the sensitivity of field populations of Helicoverpa to both Cry1Ac and Cry2Ab to detect early signs of the development of resistance to genetically modified cotton. Through the introduction of a new screening technique (F1 tests) we found that for H. armigera the assumed frequency of Cry2Ab resistance alleles in populations may be substantially (up to 6 times) higher than previously thought. In 2007/08 there was a significant increase in the frequency of Cry2Ab resistance alleles obtained using F1 screens compared to previous seasons for H. armigera. Since the introduction of Bollgard II the frequency of Cry2Ab resistance alleles obtained using F2 screens has also increased in H. punctigera. Despite these findings, Bollgard II should continue to provide excellent protection against Helicoverpa provided that the industry manages its stewardship responsibilities.

We recommend that the industry improve its compliance with the RMP particularly in terms of producing high quality refuges. Also, because late in the season Helicoverpa may be exposed to cotton that only expresses Cry2Ab, it is important to implement an effective pupae busting procedure to kill that last generation which may be enriched with Cry2Ab resistance genes.

There have been no reported field failures of Bollgard II and the occasional occurrence of threshold levels of Helicoverpa in some Bollgard II fields is not due to Bt resistance. Although survivors on Bollgard II are not currently resistant, it would be useful to control them so that they are not exposed to low doses of toxin which can select for resistance in the future. We need to verify the extent and distribution of fields with Helicoverpa survivors, and determine whether it’s possible to predict if a particular field will have a problem. Gavin Whitburn is currently working with CCA members to collect this data.

Despite a poor history in developing resistance to conventional insecticide, the industry needs to regard H. punctigera as a potential risk of developing resistance to Bt. For more information contact: Sharon Downes (Sharon.Downes@csiro.au) or Rod Mahon (Rod.Mahon@csiro.au), CSIRO Entomology