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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.
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A tug-of-war to control plant emission of an airborne alarm signal
Abstract Aphids represent a major threat to crops. Hundreds of different viruses are aphid-borne. Upon aphid attack, plants release volatile organic compounds (VOCs) as airborne alarm signals to turn on the airborne defense (AD) of neighboring plants, thereby repelling aphids as well as reducing aphid fitness and virus transmission. This phenomenon provides a critical community-wide plant protection to fend off aphids, but the underlying molecular basis remains undetermined for a long time. In a recent article, Gong et al. established theNAC2-SAMT1module as the core component regulating the emission of methyl-salicylate (MeSA), a major component of VOCs in aphid-attacked plants. Furthermore, they showed that SABP2 protein is critical for the perception of volatile MeSA signal by converting MeSA to Salicylic Acid (SA), which is the cue to elicit AD against aphids at the community level. Moreover, they showed that multiple viruses use a conserved glycine residue in the ATP-dependent helicase domain in viral proteins to shuttle NAC2 from the nucleus to the cytoplasm for degradation, leading to the attenuation of MeSA emission and AD. These findings illuminate the functional roles of key regulators in the complex MeSA-mediated airborne defense process and a counter-defense mechanism used by viruses, which has profound significance in advancing the knowledge of plant-pathogen interactions as well as providing potential targets for gene editing-based crop breeding.
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- Award ID(s):
- 2350392
- PAR ID:
- 10474476
- Publisher / Repository:
- Springer Science + Business Media
- Date Published:
- Journal Name:
- Stress Biology
- Volume:
- 3
- Issue:
- 1
- ISSN:
- 2731-0450
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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