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Check the list of papers from NScTI Citrus
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2021
Dalio, Ronaldo J. D.; Paschoal, Daniele; Arena, Gabriella D.; Magalhães, Diogo M.; Oliveira, Tiago S.; Merfa, Marcus V.; Maximo, Heros J.; Machado, Marcos A.
Hypersensitive response: From NLR pathogen recognition to cell death response Journal Article
In: Annals of Applied Biology, vol. 178, iss. 2, pp. 268-280, 2021, ISSN: 1744-7348.
Abstract | Links | BibTeX | Tags: hypersensitive response, microbe interactions, NLRs, plant, plant defence, ROS
@article{Dalio2021,
title = {Hypersensitive response: From NLR pathogen recognition to cell death response},
author = {Ronaldo J. D. Dalio and Daniele Paschoal and Gabriella D. Arena and Diogo M. Magalhães and Tiago S. Oliveira and Marcus V. Merfa and Heros J. Maximo and Marcos A. Machado},
url = {https://onlinelibrary.wiley.com/doi/full/10.1111/aab.12657 https://onlinelibrary.wiley.com/doi/abs/10.1111/aab.12657 https://onlinelibrary.wiley.com/doi/10.1111/aab.12657},
doi = {10.1111/AAB.12657},
issn = {1744-7348},
year = {2021},
date = {2021-01-01},
journal = {Annals of Applied Biology},
volume = {178},
issue = {2},
pages = {268-280},
publisher = {John Wiley & Sons, Ltd},
abstract = {A wide range of potentially plant pathogenic microorganisms are naturally present in the environment. Despite relying only on the innate immune system, plants are able to resist most of the pathogens. Plants employ a multi-layered defence system in which the first layer triggers the basal resistance (pathogen-associated molecular pattern-triggered immunity [PTI]). The second layer occurs when a resistance protein (R protein) that mostly encodes nucleotide-binding leucine-rich repeat receptors (NLRs) recognises an effector molecule secreted by an adapted pathogen, leading to effector-triggered immunity (ETI), which triggers the hypersensitive response (HR). More recently, ETI was shown to restore and potentiate PTI signalling components, leading to a robust immune response. Multiple mechanisms of regulation are employed to guarantee proper HR activation. NLR proteins can interact between them and form a heel-like pentamer that anchors to the plasma membrane. Furthermore, NLRs and other proteins can cooperate with NLRs to propagate the immune signalling. Downstream to the recognition of the pathogen by the plant, a rapid cellular response is initiated involving the generation of signalling events that precedes the HR. Here, we summarise the mechanisms involved in HR and highlight new advances in the knowledge of the immune system signalling. We also approach the role of HR threshold during infection by biotrophic, necrotrophic and hemibiotrophic pathogens and the impact in plant fitness and the community of pathogens found in the environment.},
keywords = {hypersensitive response, microbe interactions, NLRs, plant, plant defence, ROS},
pubstate = {published},
tppubtype = {article}
}
A wide range of potentially plant pathogenic microorganisms are naturally present in the environment. Despite relying only on the innate immune system, plants are able to resist most of the pathogens. Plants employ a multi-layered defence system in which the first layer triggers the basal resistance (pathogen-associated molecular pattern-triggered immunity [PTI]). The second layer occurs when a resistance protein (R protein) that mostly encodes nucleotide-binding leucine-rich repeat receptors (NLRs) recognises an effector molecule secreted by an adapted pathogen, leading to effector-triggered immunity (ETI), which triggers the hypersensitive response (HR). More recently, ETI was shown to restore and potentiate PTI signalling components, leading to a robust immune response. Multiple mechanisms of regulation are employed to guarantee proper HR activation. NLR proteins can interact between them and form a heel-like pentamer that anchors to the plasma membrane. Furthermore, NLRs and other proteins can cooperate with NLRs to propagate the immune signalling. Downstream to the recognition of the pathogen by the plant, a rapid cellular response is initiated involving the generation of signalling events that precedes the HR. Here, we summarise the mechanisms involved in HR and highlight new advances in the knowledge of the immune system signalling. We also approach the role of HR threshold during infection by biotrophic, necrotrophic and hemibiotrophic pathogens and the impact in plant fitness and the community of pathogens found in the environment.
2020
Arena, Gabriella D.; Ramos-González, Pedro Luis; Falk, Bryce W.; Casteel, Clare L.; Freitas-Astúa, Juliana; Machado, Marcos A.
Plant Immune System Activation Upon Citrus Leprosis Virus C Infection Is Mimicked by the Ectopic Expression of the P61 Viral Protein Journal Article
In: Frontiers in Plant Science, vol. 11, pp. 1188, 2020, ISSN: 1664462X.
Abstract | Links | BibTeX | Tags: Arabidopsis thaliana, Cilevirus, hypersensitive response, Jasmonic acid, Nicotiana benthamiana, plant–virus interaction, RNA-Seq, Salicylic acid
@article{Arena2020,
title = {Plant Immune System Activation Upon Citrus Leprosis Virus C Infection Is Mimicked by the Ectopic Expression of the P61 Viral Protein},
author = {Gabriella D. Arena and Pedro Luis Ramos-González and Bryce W. Falk and Clare L. Casteel and Juliana Freitas-Astúa and Marcos A. Machado},
doi = {10.3389/FPLS.2020.01188/BIBTEX},
issn = {1664462X},
year = {2020},
date = {2020-01-01},
journal = {Frontiers in Plant Science},
volume = {11},
pages = {1188},
publisher = {Frontiers Media S.A.},
abstract = {Citrus leprosis virus C (CiLV-C, genus Cilevirus, family Kitaviridae) is an atypical virus that does not spread systemically in its plant hosts. Upon its inoculation by Brevipalpus mites, only localized lesions occur, and the infection remains limited to cells around mite feeding sites. Here, we aimed to gain insights into the putative causes of viral unfitness in plants by expanding the limited knowledge of the molecular mechanisms underlying plant/kitavirid interactions. Firstly, we quantified the CiLV-C viral RNAs during the infection in Arabidopsis thaliana plants using RT-qPCR and systematized it by defining three stages of distinguishing subgenomic and genomic RNA accumulation: i) 0–24 h after infestation, ii) 2–4 days after infestation (dai), and iii) 6–10 dai. Accordingly, the global plant response to CiLV-C infection was assessed by RNA-Seq at each period. Results indicated a progressive reprogramming of the plant transcriptome in parallel to the increasing viral loads. Gene ontology enrichment analysis revealed the induction of cell growth-related processes at the early stages of the infection and the triggering of the SA-mediated pathway, ROS burst and hypersensitive response (HR) at the presymptomatic stage. Conversely, infected plants downregulated JA/ET-mediated pathways and processes involved in the primary metabolism including photosynthesis. Marker genes of unfolded protein response were also induced, suggesting a contribution of the endoplasmic reticulum stress to the cell death caused by the viral infection. Finally, we transiently expressed CiLV-C proteins in Nicotiana benthamiana plants to undertake their roles in the elicited plant responses. Expression of the CiLV-C P61 protein consistently triggered ROS burst, upregulated SA- and HR-related genes, increased SA levels, reduced JA levels, and caused cell death. Mimicry of responses typically observed during CiLV-C–plant interaction indicates P61 as a putative viral effector causing the HR-like symptoms associated with the infection. Our data strengthen the hypothesis that symptoms of CiLV-C infection might be the outcome of a hypersensitive-like response during an incompatible interaction. Consequently, the locally restricted infection of CiLV-C, commonly observed across infections by kitavirids, supports the thesis that these viruses, likely arising from an ancestral arthropod-infecting virus, are unable to fully circumvent plant defenses.},
keywords = {Arabidopsis thaliana, Cilevirus, hypersensitive response, Jasmonic acid, Nicotiana benthamiana, plant–virus interaction, RNA-Seq, Salicylic acid},
pubstate = {published},
tppubtype = {article}
}
Citrus leprosis virus C (CiLV-C, genus Cilevirus, family Kitaviridae) is an atypical virus that does not spread systemically in its plant hosts. Upon its inoculation by Brevipalpus mites, only localized lesions occur, and the infection remains limited to cells around mite feeding sites. Here, we aimed to gain insights into the putative causes of viral unfitness in plants by expanding the limited knowledge of the molecular mechanisms underlying plant/kitavirid interactions. Firstly, we quantified the CiLV-C viral RNAs during the infection in Arabidopsis thaliana plants using RT-qPCR and systematized it by defining three stages of distinguishing subgenomic and genomic RNA accumulation: i) 0–24 h after infestation, ii) 2–4 days after infestation (dai), and iii) 6–10 dai. Accordingly, the global plant response to CiLV-C infection was assessed by RNA-Seq at each period. Results indicated a progressive reprogramming of the plant transcriptome in parallel to the increasing viral loads. Gene ontology enrichment analysis revealed the induction of cell growth-related processes at the early stages of the infection and the triggering of the SA-mediated pathway, ROS burst and hypersensitive response (HR) at the presymptomatic stage. Conversely, infected plants downregulated JA/ET-mediated pathways and processes involved in the primary metabolism including photosynthesis. Marker genes of unfolded protein response were also induced, suggesting a contribution of the endoplasmic reticulum stress to the cell death caused by the viral infection. Finally, we transiently expressed CiLV-C proteins in Nicotiana benthamiana plants to undertake their roles in the elicited plant responses. Expression of the CiLV-C P61 protein consistently triggered ROS burst, upregulated SA- and HR-related genes, increased SA levels, reduced JA levels, and caused cell death. Mimicry of responses typically observed during CiLV-C–plant interaction indicates P61 as a putative viral effector causing the HR-like symptoms associated with the infection. Our data strengthen the hypothesis that symptoms of CiLV-C infection might be the outcome of a hypersensitive-like response during an incompatible interaction. Consequently, the locally restricted infection of CiLV-C, commonly observed across infections by kitavirids, supports the thesis that these viruses, likely arising from an ancestral arthropod-infecting virus, are unable to fully circumvent plant defenses.