Search for: All records

Virus-plant dynamics change over time, influencing interactions between plants and insect vectors. However, the signaling pathways and regulators that control these temporal responses remain largely unknown. In this study, we used insect performance and preference bioassays, RNA-Seq, and genetic tools to identify underlying mechanisms mediating temporal variation in plant-virus-vector interactions. We show that settlement and fecundity of the aphid vector,Myzus persicae, is increased on potato virus Y (PVY)-infectedNicotiana benthamianaplants two weeks after inoculation but not after six weeks. RNA-Seg analysis revealed transcripts related to plant defense and amino acid biosynthesis are upregulated in response to PVY infection and down regulated in response to aphid herbivory, and these patterns changed over time. Based on this analysis we identified a sesquiterpene synthase gene, terpene synthase 1 (NbTPS1), that is upregulated early in PVY infection, but not at later infection time points. Using virus-induced gene silencing and transient overexpression inN. benthamianawe demonstrate that PVY induction ofNbTPS1is required for increased aphid attraction to PVY-infected plants in the early stages of infection. Taken together, PVY temporally regulates transcriptional pathways related to plant defense responses and volatile organic compounds that influence aphid vector performance and preference. 

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 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.