RESUMEN

Transgenic Bt crops are important tools for growers to manage insect pests, but their durability is threatened by the evolution of insect resistance. Implementing a resistance monitoring program is essential to detect and mitigate resistance. For non-high-dose Bt crops, resistance monitoring is challenging, because insect control is not complete, so targeted insects and insect damage will be present even without resistance. Given these challenges, sentinel plots have been used to monitor for insect resistance to non-high-dose crops by assessing changes in the efficacy of a Bt crop over time relative to a non-Bt control. We optimized a sentinel plot resistance monitoring approach for MON 88702 ThryvOn™ cotton, a new non-high-dose Bt product targeting two sucking pest taxa-Lygus (L. lineolaris and L. hesperus) and thrips (Frankliniella fusca and F. occidentalis)-and report here on the thrips monitoring methods and results. Quantifying thrips immatures was the best metric to characterize the impact of the trait, with at least a 40-60% average reduction of thrips immatures on ThryvOn relative to the control cotton at all sites with higher thrips densities. These data can be used within a ThryvOn resistance monitoring program and represent a case study for establishing a resistance monitoring approach for a non-high-dose trait product.

RESUMEN

Host-plant resistance (HPR) is an important tool for pest management, affording both economic and environmental benefits. The mechanisms of aphid resistance in soybean are not well understood, but likely involve the induction of the jasmonic acid (JA) pathway, and possibly other phytohormone signals involved in plant defense responses. Despite the efficacy of aphid resistance in soybean, virulent aphids have overcome this resistance through mostly unknown mechanisms. Here, we have used metabolomic tools to define the role of plant phytohormones, especially the JA pathway, in regulating interactions between aphid-resistant soybean and virulent aphids. We hypothesized that virulent aphids avoid or suppress the JA pathway to overcome aphid resistance. Our results suggested that aphid-resistant soybean increased accumulation of JA-isoleucine (JA-Ile) only when infested with avirulent aphids; virulent aphids did not cause induction of JA-Ile. Further, applying JA-Ile to aphid-resistant soybean reduced subsequent virulent aphid populations. The concentrations of other phytohormones remained unchanged due to aphid feeding, highlighting the importance of JA-Ile in this interaction. These results increase our knowledge of soybean resistance mechanisms against soybean aphids and contribute to our understanding of aphid virulence mechanisms, which will in turn promote the durability of HPR.

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RESUMEN

In agricultural systems, crops equipped with host-plant resistance (HPR) have enhanced protection against pests, and are used as a safe and sustainable tool in pest management. In soybean, HPR can control the soybean aphid (Aphis glycines), but certain aphid populations have overcome this resistance (i.e., virulence). The molecular mechanisms underlying aphid virulence to HPR are unknown, but likely involve effector proteins that are secreted by aphids to modulate plant defenses. Another mechanism to facilitate adaptation is through the activity of transposable elements, which can become activated by stress. In this study, we performed RNA sequencing of virulent and avirulent soybean aphids fed susceptible or resistant (Rag1 + Rag2) soybean. Our goal was to better understand the molecular mechanisms underlying soybean aphid virulence. Our data showed that virulent aphids mostly down regulate putative effector genes relative to avirulent aphids, especially when aphids were fed susceptible soybean. Decreased expression of effectors may help evade HPR plant defenses. Virulent aphids also transcriptionally up regulate a diverse set of transposable elements and nearby genes, which is consistent with stress adaptation. Our work demonstrates two mechanisms of pest adaptation to resistance, and identifies effector gene targets for future functional testing.

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