Monitoring to Manage Resistance to Bt Toxins

Date Issued:2016-06-30

Abstract

The industry is entering a critical period in managing resistance to Bt-cotton. One technology provider is about to release their 3rd generation product which is based on the current two gene varieties (Cry1Ac, Cry2Ab) plus Vip3A. It is possible that in the near future other technology providers will enter the market. If more than one Bt-cotton product is commercial, at least in the short term, it is likely that larvae will be exposed to the same or different varieties of Bt toxins within the 3 classes that are currently included in the resistance monitoring program: Cry1A, Cry2A and Vip3A. Resistant insects are likely to tolerate different varieties of toxins within the same class, so for instance, resistance frequencies for Cry2Aa should be the same as those for Cry2Ab. The development of robust resistance management plans (RMPs) for these technologies depends critically on the frequencies of common resistances to these key classes of Bt toxins.

In this project we achieved our main planned outcome of rigorously assessing the sensitivity of field populations of Helicoverpa to Cry1Ac, Cry2Ab and Vip3A toxins to detect early signs of the development of resistance to genetically modified cotton. It was utilised in mathematical models that evaluated the risk of resistance evolving to three toxin (Cry1Ac, Cry2Ab, Vip3A) cotton and ultimately to the development of a Resistance Management Plan for Bollgard III cotton.

In H. punctigera the proportion of individuals in the population that are heterozygous (rS) for the cry1Ac resistance gene is 2% (based on F1 data: 1% of alleles is equivalent to 2% of individuals). Cry2Ab resistance genes were present at detectable levels before Bollgard II® was widespread. In H. armigera the proportion of individuals in the population that are heterozygous for the cry2Ab resistance gene is 4%. In H. punctigera the proportion of individuals in the population that are heterozygous for the cry2Ab resistance gene is 3%. Vip3A resistance genes are present at detectable levels before Bollgard III® is due to be released (in 2016/17). In H. armigera and H. punctigera the proportion of individuals in the population that are heterozygous for the vip3A resistance gene is 2%.

Individuals that are homozygous for the Cry1Ac allele (H. punctigera), Cry2Ab allele (H. armigera and H. punctigera) or Vip3A allele (H. armigera and H. punctigera) have been detected since F1 screens commenced; these frequencies are not significantly different from what is expected based on the frequencies of heterozygotes.

No new dominant resistances to Cry1Ac, Cry2Ab or Vip3A have been detected.

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 a physiological resistance to Bt toxins. A survey of crop consultants suggests that the presence of medium-large larvae in Bollgard II® is (1) not increasing (from 2005/06 to 2015/16); (2) widespread among valleys and climatic regions; and (3) usually controlled especially recently. Thresholds are equally likely to be driven by numbers of medium-large versus small larvae. Bollgard II is sometimes sprayed for larvae below threshold.

Moving forward we suggest continuing with the shift in focus toward known resistances and screening for any new dominant resistances. New changes include screening every other year and shift towards using molecular tools to assist bioassays.

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