No sustainable GMO solution to Bt-resistant pests

Stacked-trait Bt crops and Monsanto’s new gene-silencing technology are unlikely to provide a lasting solution to resistant crop-munching pests, reports Claire Robinson



GM Bt insecticidal maize has fallen victim to the armyworm pest in Brazil, as GMWatch reported early in 2015.



Two types of maize targeting the fall armyworm (among other pests) are widely planted in Brazil:

* MON810 event with the Cry1Ab Bt toxin gene (Cry1Ab maize)

* TC1507 event with the cry1F Bt toxin gene (Cry1F maize).



As fall armyworm has developed resistance to MON810 Cry1Ab maize, Cry1F maize has replaced it as a supposed solution.



But a new study (abstract below) by Brazilian and US scientists, including several from Monsanto, shows that neither maize is successfully combatting the fall armyworm pest, which has rapidly developed resistance to GM Bt technology.



And the GM industry appears to have no sustainable solution to the resistance problem in the pipeline.

Main findings of new study

The new study found that:



* Fall armyworm larvae are only “moderately susceptible” to the Cry1Ab Bt insecticidal toxin protein expressed in MON810 maize.



* Efficacy of MON810 in combating fall armyworm is decreasing over time as the pest develops resistance to the Cry1Ab Bt toxin. Farmers have to spray insecticides to prevent serious damage to the crop.



* GM maize expressing another Bt toxin insecticidal protein, Cry1F, is currently planted in Brazil. But the fall armyworm pest has also developed widespread resistance to Cry1F in Brazil and Puerto Rico.



* The “refuge strategy”, recommended to delay resistance to Bt crops, is failing, though it’s also been poorly implemented in Brazil. The refuge strategy consists of planting areas of non-Bt crops near Bt crop fields to try to ensure that some of the pests remain susceptible to Bt toxin and are able to mate with Bt-resistant pests, producing Bt-susceptible progeny. But the delayed development of larvae reared on MON810 compared with larvae reared on non-Bt maize means that it may be hard for Bt-resistant pests to find Bt-susceptible pests to mate with, thus potentially undermining the refuge strategy and hastening pest resistance.



* MON810 contains only a moderate dose of Bt toxin, meaning that some insect pests will eat the Bt maize and survive, passing on their resistance genes and increasing the problem of pest resistance.



* Because maize is grown in Brazil in two consecutive crops in the same season, fall armyworm populations can build up over time. Also, the pest has multiple food sources, increasing its survivability.



* The above factors favour resistance to chemical insecticides and Bt crops developing in fall armyworm in Brazil.



* The Cry1F Bt maize planted in Brazil does not contain a high enough dose of Bt toxin to enable successful control of fall armyworm.



* Cross-resistance between different Bt toxin (Cry) proteins is expected to occur in fall armyworm, based on experimental studies.



* The researchers were unable to conclude whether the fall armyworm’s resistance to Cry1Ab was due to exposure to MON810 or to other Bt toxins, such as Cry1F (cross-resistance).

Potential solutions?

As a solution to these problems, the authors recommend, “Technologies combining multiple novel insecticidal traits with no cross-resistance to the current Cry1 proteins and high activity against the same target pests should be pursued in Brazil and similar environments.”



These are so-called stacked-trait Bt crops, containing multiple Bt toxins. The aim is that pests that are not killed by one type of Bt toxin will be killed by another in the “stack” of Bt traits.



In addition, Monsanto’s new maize, which combines Bt toxin with RNAi (RNA interference) technology targeting the rootworm pest, is currently in the USDA deregulation pipeline. The RNAi works by silencing or manipulating genes within the insect that it needs to survive, thus killing it.

Will it work?

We invited Dr Doug Gurian-Sherman, senior scientist at the Center for Food Safety, to comment on whether these proposed solutions are likely to work.



Dr Gurian-Sherman said:



“Other research shows that several Bt stacks that are intended to delay resistance to Bt can actually have cross-resistance, and are therefore not effective as stacks. This has also been shown for other insects as well, for example, the cotton bollworm.



“Cross-resistance has not been shown between several Cry proteins, e.g. Cry3 and Cry34/35 for rootworm, and some other combinations for Lepidoptera [moth] control. But that does not mean it cannot happen. Several different mechanisms of resistance have already been found, but it is possible that currently unknown mechanisms for cross-resistance may develop.



“Even if cross-resistance does not occur, several mechanisms can develop sequentially to provide resistance to several Bts if they are not deployed carefully.



“In fact, for stacks with several different toxins (or other mechanisms like RNAi), resistance to one of the components in the stack is often already prevalent when the stacked variety is released commercially. This means that in reality, a stack of two genes will really act as only a single gene – the one for which resistance is not widespread – and the stack will not delay resistance any longer than a single gene.



“This seems to be the common occurrence at this point – for example, with rootworm Bt or GM herbicide-tolerance genes – perhaps because the time and cost needed to develop each gene means that they will usually be released sequentially rather than several at once.



“Additionally, neither Monsanto’s Bt against rootworm nor its new anti-rootworm RNAi corn provide a high enough dose to be effective for resistance prevention when the current mandated refuge strategy, intended to prevent or delay resistance, is applied. Indeed, resistance to Monsanto's Cry3Bb1 developed after just a few years. With most insect pests (e.g. bollworm, rootworm, armyworm), when a high enough dose of Bt is not provided by the GM Bt crop, resistance has developed within 5–10 years or less.”

Gene-silencing technology to the rescue?

Could the RNAi technology make up for any inadequacy in the Bt content?



Dr Gurian-Sherman said:



“We have no experience with commercial RNAi transgenics for insect control, but there is no reason to think that resistance can't develop as quickly as with other types of control, such as pesticides or other GE.



“Pests have their own native mechanisms for manipulating or detoxifying chemicals or avoiding harm from those chemicals, which they use to develop resistance to chemical insecticides and Bt insecticidal toxins. These include genetic mutations and rare variations in existing genes (alleles). I am suggesting that similar processes will operate with RNAi.



“Insects have native RNAi genetics, which regulate and manipulate these small RNA molecules. RNAi, while new as a means of controlling pests, is not new to pests, but is part of their native biology. Insects have been adept at developing resistance to chemical insecticides, in part because they have many biochemical mechanisms to manipulate (metabolize) many kinds of chemicals, and because natural mutations occur or already exist that make the target of the chemicals immune to them – and these mechanisms can be adapted to provide resistance. In the same vein, insects are also biochemically familiar with RNAi.



“Unless there are big changes in terms of providing robust means of preventing or delaying resistance, resistance to RNAi will likely develop before long. And the history with Bt so far is that for traits that do not provide a high dose of the pesticide, adequate resistance prevention has not been mandated by regulations.”

Dustbin of history

In short, Monsanto’s new gene-silencing solution to pest resistance to GM Bt crops appears doomed to go the same way as its GM Bt crops – into the dustbin of agricultural history.



In the meantime, scientists warn that eating GM crops and other products containing gene-silencing technology could do serious damage to animal and human consumers, as well as to ecosystems.

—

Field-evolved resistance to Cry1Ab maize by Spodoptera frugiperda in Brazil

Omoto, C., Bernardi, O., Salmeron, E., Sorgatto, R. J., Dourado, P. M., et al. (2015).

Pest Management Science. DOI: 10.1002/ps.4201

http://onlinelibrary.wiley.com/doi/10.1002/ps.4201/abstract



Abstract



Background



The first Bt maize in Brazil was launched in 2008 and contained the MON 810 event, which expresses Cry1Ab protein. Although the Cry1Ab dose in MON 810 is not high against fall armyworm (FAW), Spodoptera frugiperda (J.E. Smith), MON 810 provided commercial levels of control. To support insect resistance management in Brazil, the baseline and ongoing susceptibility of FAW was examined using protein bioassays, and the level of control and life history parameters of FAW were evaluated on MON 810 maize.



Results



Baseline diet-overlay assays with Cry1Ab (16 µg cm−2) caused 76.3% mortality to field FAW populations sampled in 2009. Moderate mortality (48.8%) and significant growth inhibition (88.4%) were verified in leaf disc bioassays. In greenhouse trials, MON 810 had significantly less damage than non-Bt maize. The surviving FAW larvae on MON 810 (22.4% ) had a 5.5-day increase in life cycle time and a 24% reduction in population growth rate. Resistance monitoring (2010–2015) showed a significant reduction in Cry1Ab susceptibility of FAW over time. Additionally, a significant reduction in the field efficacy of MON 810 maize against FAW was observed in different regions from crop season 2009 to 2013.



Conclusions



The decrease susceptibility to Cry1Ab was expected, but the specific contributions to this resistance by MON 810 maize cannot be distinguished from cross-resistance to Cry1Ab caused by exposure to Cry1F maize. Technologies combining multiple novel insecticidal traits with no cross resistance to the current Cry1 proteins and high activity against the same target pests should be pursued in Brazil and similar environments.