The African maize stemborer's resistance to Bt crops reveals evolution in action and challenges modern agricultural practices
In the vast maize fields of South Africa, a quiet but significant evolutionary drama is unfolding. The African maize stemborer, Busseola fusca, a seemingly unremarkable moth, is steadily outmaneuvering one of modern agriculture's most powerful innovations: genetically modified Bt maize. This isn't just a story about a crop pest; it's a real-time lesson in evolution that threatens food security and challenges our approach to agricultural technology.
By 2017-2018, farmers in KwaZulu-Natal began noticing B. fusca larvae surviving on MON 89034 maize plants, which contain two different Bt proteins designed to prevent resistance.
First resistance to Cry1Ab protein was documented in 2006, just seven years after Bt maize's introduction in South Africa.
For decades, Bt maize—genetically engineered to produce proteins from the bacterium Bacillus thuringiensis (Bt) that are toxic to insect pests—has been a cornerstone of pest control in South African agriculture. First introduced in the late 1990s, it offered farmers a powerful weapon against destructive stemborers without chemical insecticides. But nature adapts. In 2006, just seven years after Bt maize's introduction, scientists documented the first signs of Busseola fusca resistance to the Cry1Ab protein in MON 810 maize. The agricultural community responded by introducing a more advanced variety—MON 89034—containing two different Bt proteins (Cry1A.105 and Cry2Ab2), hoping this dual-toxin approach would overcome resistance. For a while, it worked. But by the 2017-2018 growing season, farmers in KwaZulu-Natal began noticing something alarming—B. fusca larvae surviving on the supposedly protected plants. The quiet rebellion had begun, and science is now racing to understand its implications for the future of crop protection 1 3 .
To understand the significance of this resistance, we must first appreciate how Bt technology works. Bt maize is genetically engineered to produce proteins originally derived from the Bacillus thuringiensis bacterium. These "Cry" proteins are toxic to specific insect pests but harmless to humans, wildlife, and beneficial insects. When susceptible larvae like Busseola fusca feed on Bt maize tissues, the Cry proteins bind to specific receptors in their gut, creating pores that ultimately kill the insects.
Widespread deployment of Bt crops creates immense selection pressure—individual insects with natural resistance to the Bt proteins survive and reproduce, passing those resistance traits to their offspring.
First commercial planting of Cry1Ab maize (MON 810) in South Africa
First documentation of B. fusca resistance to Cry1Ab (7 years after introduction)
Introduction of second-generation Bt maize MON 89034 (containing Cry1A.105 and Cry2Ab2)
First reports of B. fusca infestations on MON 89034 in KwaZulu-Natal province
Reports of B. fusca damage to MON 89034 expand to Mpumalanga province
Scientific confirmation of Cry2Ab2 resistance in three South African populations
The agricultural industry's strategy to delay resistance has centered on the "high-dose/refuge" approach. This involves engineering plants to produce Bt toxins at doses high enough to kill even partially resistant insects, while mandating that farmers plant "refuges" of non-Bt crops nearby. These refuges maintain populations of susceptible insects that can mate with any resistant survivors from Bt fields, diluting resistance genes in the next generation 2 5 .
Pyramided Bt crops like MON 89034, which express two distinct Bt toxins, were supposed to provide additional protection. The theory was that insects resistant to one toxin would be killed by the second, significantly slowing resistance evolution. However, as we'll see, this theory has met with unexpected challenges in the case of Busseola fusca 1 .
When reports of B. fusca infestations in Bt maize fields surfaced from multiple South African provinces, a team of scientists embarked on a systematic investigation to determine what was happening. Their 2024 study, published in Pest Management Science, represents a crucial piece of detective work in the ongoing resistance mystery 1 .
Researchers incorporated purified Cry2Ab2 protein into artificial diet to test protein efficacy in isolation.
Larvae from different populations were monitored for survival and growth rates when exposed to Bt proteins.
Larvae were placed directly on MON 89034 leaf tissue and observed for seven days to confirm findings.
| Bt Protein | Efficacy Status | Notes |
|---|---|---|
| Cry1Ab (MON 810) | Low | Resistance evolved by 2006 |
| Cry1A.105 (in MON 89034) | Low | Ineffective against all populations |
| Cry2Ab2 (in MON 89034) | Variable | Only functional toxin against B. fusca |
The results were telling—and alarming. While larvae from most populations showed 100% mortality when exposed to Cry2Ab2 in artificial diet, those from the three problem areas survived at significantly higher rates. Even more revealing was what happened when larvae were placed directly on MON 89034 leaf tissue: after seven days, a staggering 75-91% of larvae from the problem populations survived, compared to just 0.4-9.6% from other populations 1 .
Perhaps the most surprising discovery was that one of the two Bt proteins in MON 89034—Cry1A.105—proved ineffective against all B. fusca populations tested, including those known to be susceptible to Bt toxins. This finding transformed the understanding of MON 89034's protective mechanism—rather than being a true two-toxin pyramid against B. fusca, it was effectively relying on just Cry2Ab2 1 3 .
Understanding and combating resistance requires sophisticated tools and methods. The researchers investigating Busseola fusca resistance employ a range of specialized approaches in their work:
These customized laboratory diets serve as the foundation for resistance monitoring. Scientists can incorporate specific Bt proteins at precise concentrations to determine toxicity levels and establish baseline susceptibility.
Maintaining viable colonies of both susceptible and field-collected B. fusca populations is essential for comparative studies. These facilities require precise environmental controls to ensure consistent experimental subjects.
While artificial diets provide controlled conditions, whole plant assays offer critical validation. Researchers infest maize plants with known numbers of larvae, then track damage and survival rates over time.
Systematic collection of larvae from multiple geographic locations allows researchers to track the emergence and spread of resistance. This early-warning system detected the initial Cry2Ab2 resistance.
These tools collectively enable scientists to not only identify resistance after it emerges but to understand the mechanisms behind it and potentially predict its future evolution 1 5 .
The Busseola fusca story extends far beyond laboratory toxicity tests. The insect's natural behavior plays a crucial role in how resistance develops and spreads—and why certain resistance management strategies may fail.
Research has revealed that B. fusca larvae can detect Bt toxins in maize plants and show feeding avoidance. Both resistant and susceptible neonate larvae are more likely to abandon Bt maize plants than conventional non-Bt plants.
Studies show that B. fusca larvae don't typically migrate long distances—most move no further than two plants from their natal plant. This becomes significant in the context of seed mixtures.
The failure of MON 89034 as a true pyramid variety against B. fusca—with Cry1A.105 proving ineffective—has created what scientists call a "single-mode-of-action technology" against this pest. This carries an inherent high risk for resistance evolution, as the insects only need to develop resistance to one functional toxin rather than two 1 3 .
More comprehensive sampling to detect resistance earlier
Moving away from seed mixtures to minimize larval movement
Combining crop rotation, biological controls, and insecticides
The case of Busseola fusca demonstrates that technological solutions alone cannot overcome ecological and evolutionary forces. Sustainable pest management requires understanding insect behavior, ecology, and the relentless power of natural selection 1 2 5 .
The quiet rebellion of Busseola fusca against genetically engineered maize serves as a living laboratory of evolution in action. It demonstrates that despite our most advanced agricultural technologies, natural selection continues to operate with relentless efficiency. What makes this case particularly compelling is that it represents one of the earliest documented examples of field-evolved resistance to a pyramided Bt crop anywhere in the world.
Sustainable agriculture requires respect for biological principles and the development of management strategies that work with, rather than against, evolutionary realities.
The implications extend far beyond South African maize fields. They remind us that sustainable agriculture requires respect for biological principles and the development of management strategies that work with, rather than against, evolutionary realities. As research continues, the story of Busseola fusca offers valuable lessons for managing other pests in other crops—lessons about the inevitability of resistance, the importance of understanding insect behavior, and the need for diverse approaches to pest control.
In the ongoing co-evolutionary dance between crops and their pests, the music never stops. The rebellion of the African maize stemborer reminds us that our technological solutions must be as adaptive and resilient as the pests we aim to control. The future of crop protection may lie not in single silver bullets, but in integrated strategies that acknowledge a fundamental truth: in agriculture, as in nature, change is the only constant 1 3 5 .