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Abstract Plant viruses both trigger and inhibit host plant defense responses, including defenses that target their insect vectors, such as aphids. Turnip mosaic viru (TuMV) infection and its protein, NIa-Pro (nuclear inclusion protease a), suppress aphid-induced plant defenses, however the mechanisms of this suppression are still largely unknown. In this study, we determined that NIa-Pro’s protease activity is required to increase aphid performance on host plants and that 40 transcripts with predicted NIa-Pro cleavage sequences are regulated in Arabidopsis plants challenged with aphids and/or virus compared to healthy controls. One of the candidates, MEDIATOR 16 (MED16), regulates the transcription of ethylene (ET)/jasmonic acid (JA)-dependent defense responses against necrotrophic pathogens. We show that a nuclear localization signal is removed from MED16 by specific proteolytic cleavage in virus-infected plants and in plants overexpressing NIa-Pro in the presence of aphids. Although some cleavage was occasionally detected in the absence of virus infection, it occurred at a much higher rate in plants that were virus-infected or overexpressing NIa-Pro, especially when aphids were also present. This suggests MED16 functions in the nucleus may be impacted in virus infected plants. Consistent with this, induction of the MED16-dependent transcript ofPLANT DEFENSIN 1.2 (PDF1.2), was reduced in virus-infected plants and in plants expressing NIa-Pro compared to controls, but not in plants expressing NIa-Pro C151A that lacks its protease activity. Finally, we show the performance of both the virus and the aphid vector was enhanced onmed16mutant Arabidopsis compared to controls. Overall, this study demonstrates MED16 regulates defense responses against both the virus and the aphid and provides insights into the mechanism by which TuMV suppresses anti-virus and anti-herbivore defenses. 

Abstract Hemipterans (such as aphids, whiteflies, and leafhoppers) are some of the most devastating insect pests due to the numerous plant pathogens they transmit as vectors, which are primarily viral. Over the past decade, tremendous progress has been made in broadening our understanding of plant–virus–vector interactions, yet on the molecular level, viruses and vectors have typically been studied in isolation of each other until recently. From that work, it is clear that both hemipteran vectors and viruses use effectors to manipulate host physiology and successfully colonize a plant and that co-evolutionary dynamics have resulted in effective host immune responses, as well as diverse mechanisms of counterattack by both challengers. In this review, we focus on advances in effector-mediated plant–virus–vector interactions and the underlying mechanisms. We propose that molecular synergisms in vector–virus interactions occur in cases where both the virus and vector benefit from the interaction (mutualism). To support this view, we show that mutualisms are common in virus–vector interactions and that virus and vector effectors target conserved mechanisms of plant immunity, including plant transcription factors, and plant protein degradation pathways. Finally, we outline ways to identify true effector synergisms in the future and propose future research directions concerning the roles effectors play in plant–virus–vector interactions. 

Potyviral genomes encode just 11 major proteins and multifunctionality is associated with most of these proteins at different stages of the virus infection cycle. Some potyviral proteins modulate phytohormones and protein degradation pathways and have either pro- or anti-viral/insect vector functions. Our previous work demonstrated that the potyviral protein 6K1 has an antagonistic effect on vectors when expressed transiently in host plants, suggesting plant defenses are regulated. However, to our knowledge the mechanisms of how 6K1 alters plant defenses and how 6K1 functions are regulated are still limited. Here we show that the 6K1 from Turnip mosaic virus (TuMV) reduces the abundance of transcripts related to jasmonic acid biosynthesis and cysteine protease inhibitors when expressed in Nicotiana benthamiana relative to controls. 6K1 stability increased when cysteine protease activity was inhibited chemically, showing a mechanism to the rapid turnover of 6K1 when expressed in trans. Using RNAseq, qRT-PCR, and enzymatic assays, we demonstrate TuMV reprograms plant protein degradation pathways on the transcriptional level and increases 6K1 stability at later stages in the infection process. Moreover, we show 6K1 decreases plant protease activity in infected plants and increases TuMV accumulation in systemic leaves compared to controls. These results suggest 6K1 has a pro-viral function in addition to the anti-insect vector function we observed previously. Although the host targets of 6K1 and the impacts of 6K1-induced changes in protease activity on insect vectors are still unknown, this study enhances our understanding of the complex interactions occurring between plants, potyviruses, and vectors. 

Abstract Animals derive resources from their diet and allocate them to organismal functions such as growth, maintenance, reproduction, and dispersal. How variation in diet quality can affect resource allocation to life-history traits, in particular those important to locomotion and dispersal, is poorly understood. We hypothesize that, particularly for specialist herbivore insects that are in co-evolutionary arms races with host plants, changes in host plant will impact performance. From their coevolutionary arms-race with plants, to a complex migratory life history, Monarch butterflies are among the most iconic insect species worldwide. Population declines initiated international conservation efforts involving the replanting of a variety of milkweed species. However, this practice was implemented with little regard for how diverse defensive chemistry of milkweeds experienced by monarch larvae may affect adult fitness traits. We report that adult flight muscle investment, flight energetics, and maintenance costs depend on the host plant species of larvae, and correlate with concentration of milkweed-derived cardenolides sequestered by adults. Our findings indicate host plant species can impact monarchs by affecting fuel requirements for flight. 

Abstract Background Maize ( Zea mays L.) is a major cereal crop, with the United States accounting for over 40% of the worldwide production. Corn leaf aphid [CLA; Rhopalosiphum maidis (Fitch)] is an economically important pest of maize and several other monocot crops. In addition to feeding damage, CLA acts as a vector for viruses that cause devastating diseases in maize. We have shown previously that the maize inbred line Mp708, which was developed by classical plant breeding, provides heightened resistance to CLA. However, the transcriptomic variation conferring CLA resistance to Mp708 has not been investigated. Results In this study, we contrasted the defense responses of the resistant Mp708 genotype to those of the susceptible Tx601 genotype at the transcriptomic (mRNA-seq) and volatile blend levels. Our results suggest that there was a greater transcriptomic remodeling in Mp708 plants in response to CLA infestation compared to the Tx601 plants. These transcriptomic signatures indicated an activation of hormonal pathways, and regulation of sesquiterpenes and terpenoid synthases in a constitutive and inducible manner. Transcriptomic analysis also revealed that the resistant Mp708 genotype possessed distinct regulation of ethylene and jasmonic acid pathways before and after aphid infestation. Finally, our results also highlight the significance of constitutive production of volatile organic compounds (VOCs) in Mp708 and Tx601 plants that may contribute to maize direct and/or indirect defense responses. Conclusions This study provided further insights to understand the role of defense signaling networks in Mp708’s resistance to CLA.