scholarly journals Cell Death Triggered by a Putative Amphipathic Helix of Radish mosaic virus Helicase Protein Is Tightly Correlated With Host Membrane Modification

2015 ◽  
Vol 28 (6) ◽  
pp. 675-688 ◽  
Author(s):  
Masayoshi Hashimoto ◽  
Ken Komatsu ◽  
Ryo Iwai ◽  
Takuya Keima ◽  
Kensaku Maejima ◽  
...  
Keyword(s):  
Cell Death ◽  
Mosaic Virus ◽  
Defense Responses ◽  
Plant Viruses ◽  
Amphipathic Helix ◽  
Membrane Structures ◽  
Membrane Modification ◽  
Systemic Necrosis ◽  
Amino Terminal ◽  
Er Membrane

Systemic necrosis is one of the most severe symptoms caused by plant RNA viruses. Recently, systemic necrosis has been suggested to have similar features to a defense response referred to as the hypersensitive response (HR), a form of programmed cell death. In virus-infected plant cells, host intracellular membrane structures are changed dramatically for more efficient viral replication. However, little is known about whether this replication-associated membrane modification is the cause of the symptoms. In this study, we identified an amino-terminal amphipathic helix of the helicase encoded by Radish mosaic virus (RaMV) (genus Comovirus) as an elicitor of cell death in RaMV-infected plants. Cell death caused by the amphipathic helix had features similar to HR, such as SGT1-dependence. Mutational analyses and inhibitor assays using cerulenin demonstrated that the amphipathic helix–induced cell death was tightly correlated with dramatic alterations in endoplasmic reticulum (ER) membrane structures. Furthermore, the cell death–inducing activity of the amphipathic helix was conserved in Cowpea mosaic virus (genus Comovirus) and Tobacco ringspot virus (genus Nepovirus), both of which are classified in the family Secoviridae. Together, these results indicate that ER membrane modification associated with viral intracellular replication may be recognized to prime defense responses against plant viruses.

scholarly journals Viral-Induced Systemic Necrosis in Plants Involves Both Programmed Cell Death and the Inhibition of Viral Multiplication, Which Are Regulated by Independent Pathways

2010 ◽  
Vol 23 (3) ◽  
pp. 283-293 ◽  
Author(s):  
Ken Komatsu ◽  
Masayoshi Hashimoto ◽  
Johji Ozeki ◽  
Yasuyuki Yamaji ◽  
Kensaku Maejima ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Viral Infection ◽  
Expression Patterns ◽  
Plant Viruses ◽  
Virus Multiplication ◽  
Mitogen Activated Protein Kinase ◽  
Systemic Necrosis ◽  
Viral Multiplication ◽  
Plantago Asiatica

Resistant plants respond rapidly to invading avirulent plant viruses by triggering a hypersensitive response (HR). An HR is accompanied by a restraint of virus multiplication and programmed cell death (PCD), both of which have been observed in systemic necrosis triggered by a successful viral infection. Here, we analyzed signaling pathways underlying the HR in resistance genotype plants and those leading to systemic necrosis. We show that systemic necrosis in Nicotiana benthamiana, induced by Plantago asiatica mosaic virus (PlAMV) infection, was associated with PCD, biochemical features, and gene expression patterns that are characteristic of HR. The induction of necrosis caused by PlAMV infection was dependent on SGT1, RAR1, and the downstream mitogen-activated protein kinase (MAPK) cascade involving MAPKKKα and MEK2. However, although SGT1 and RAR1 silencing led to an increased accumulation of PlAMV, silencing of the MAPKKKα-MEK2 cascade did not. This observation indicates that viral multiplication is partly restrained even in systemic necrosis induced by viral infection, and that this restraint requires SGT1 and RAR1 but not the MAPKKKα-MEK2 cascade. Similarly, although both SGT1 and MAPKKKα were essential for the Rx-mediated HR to Potato virus X (PVX), SGT1 but not MAPKKKα was involved in the restraint of PVX multiplication. These results suggest that systemic necrosis and HR consist of PCD and a restraint of virus multiplication, and that the latter is induced through unknown pathways independent from the former.

scholarly journals Genome-Wide Identification Reveals That Nicotiana benthamiana Hypersensitive Response (HR)-Like Lesion Inducing Protein 4 (NbHRLI4) Mediates Cell Death and Salicylic Acid-Dependent Defense Responses to Turnip Mosaic Virus

2021 ◽  
Vol 12 ◽  
Author(s):  
Xinyang Wu ◽  
Yuchao Lai ◽  
Shaofei Rao ◽  
Lanqing Lv ◽  
Mengfei Ji ◽  
...  
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Mosaic Virus ◽  
Hypersensitive Response ◽  
Nicotiana Benthamiana ◽  
Defense Responses ◽  
Turnip Mosaic Virus ◽  
Genome Wide ◽  
Transient Overexpression ◽  
Basal Immunity

Hypersensitive response (HR)-like cell death is an important mechanism that mediates the plant response to pathogens. In our previous study, we reported that NbHIR3s regulate HR-like cell death and basal immunity. However, the host genes involved in HR have rarely been studied. Here, we used transcriptome sequencing to identify Niben101Scf02063g02012.1, an HR-like lesion inducing protein (HRLI) in Nicotiana benthamiana that was significantly reduced by turnip mosaic virus (TuMV). HRLIs are uncharacterized proteins which may regulate the HR process. We identified all six HRLIs in N. benthamiana and functionally analyzed Niben101Scf02063g02012.1, named NbHRLI4, in response to TuMV. Silencing of NbHRLI4 increased TuMV accumulation, while overexpression of NbHRLI4 conferred resistance to TuMV. Transient overexpression of NbHRLI4 caused cell death with an increase in the expression of salicylic acid (SA) pathway genes but led to less cell death level and weaker immunity in plants expressing NahG. Thus, we have characterized NbHRLI4 as an inducer of cell death and an antiviral regulator of TuMV infection in a SA-mediated manner.

scholarly journals The Plant Gene CCD1 Selectively Blocks Cell Death During the Hypersensitive Response to Cauliflower Mosaic Virus Infection

2005 ◽  
Vol 18 (3) ◽  
pp. 212-219 ◽  
Author(s):  
John Cawly ◽  
Anthony B. Cole ◽  
Lóránt Király ◽  
Wenping Qiu ◽  
James E. Schoelz
Keyword(s):  
Cell Death ◽  
Mosaic Virus ◽  
Hypersensitive Response ◽  
Plant Pathogens ◽  
Plant Viruses ◽  
Cauliflower Mosaic Virus ◽  
Plant Gene ◽  
Cell Death Pathway ◽  
Resistance Pathway ◽  
Key Characteristics

The P6 protein of Cauliflower mosaic virus (CaMV) W260 elicits a hypersensitive response (HR) on inoculated leaves of Nicotiana edwardsonii. This defense response, common to many plant pathogens, has two key characteristics, cell death within the initially infected tissues and restriction of the pathogen to this area. We present evidence that a plant gene designated CCD1, originally identified in N. bigelovii, can selectively block the cell death pathway during HR, whereas the resistance pathway against W260 remains intact. Suppression of cell death was evident not only macroscopically but also microscopically. The suppression of HR-mediated cell death was specific to CaMV, as Tobacco mosaic virus was able to elicit HR in the plants that contained CCD1. CCD1 also blocks the development of a systemic cell death symptom induced specifically by the P6 protein of W260 in N. clevelandii. Introgression of CCD1 from N. bigelovii into N. clevelandii blocked the development of systemic cell death in response to W260 infection but could not prevent systemic cell death induced by Tomato bushy stunt virus. Thus, CCD1 blocks both local and systemic cell death induced by P6 of W260 but does not act as a general suppressor of cell death induced by other plant viruses. Furthermore, experiments with CCD1 provide further evidence that cell death could be uncoupled from resistance in the HR of Nicotiana edwardsonii to CaMV W260.

Capsicum annum Hsp26.5 promotes defense responses against RNA viruses via ATAF2 but is hijacked as a chaperone for tobamovirus movement protein

2020 ◽  
Vol 71 (19) ◽  
pp. 6142-6158
Author(s):  
Siew-Liang Foong ◽  
Kyung-Hee Paek
Keyword(s):  
Mosaic Virus ◽  
Defense Response ◽  
Rna Viruses ◽  
Defense Responses ◽  
Plant Viruses ◽  
Pepper Mild Mottle Virus ◽  
Movement Proteins ◽  
Pathogenesis Related ◽  
Pathogenesis Related Gene ◽  
Rna Interaction

Abstract The expression of Capsicum annuum HEAT SHOCK PROTEIN 26.5 (CaHsp26.5) was triggered by the inoculation of Tobacco mosaic virus pathotype P0 (TMV-P0) but its function in the defense response of plants is unknown. We used gene silencing and overexpression approaches to investigate the effect of CaHsp26.5 expression on different plant RNA viruses. Moreover, we performed protein–protein and protein–RNA interaction assays to study the mechanism of CaHsp26.5 function. CaHsp26.5 binding to a short poly-cytosine motif in the 3'-untranslated region of the genome of some viruses triggers the expression of several defense-related genes such as PATHOGENESIS-RELATED GENE 1 with the help of a transcription factor, NAC DOMAIN-CONTAINING PROTEIN 81 (ATAF2). Thus, an elevated CaHsp26.5 level was accompanied by increased plant resistance against plant viruses such as Cucumber mosaic virus strain Korea. However, the movement proteins of Pepper mild mottle virus pathotype P1,2,3 and TMV-P0 were shown to be able to interact with CaHsp26.5 to maintain the integrity of their proteins. Our work shows CaHsp26.5 as a positive player in the plant defense response against several plant RNA viruses. However, some tobamoviruses can hijack CaHsp26.5’s chaperone activity for their own benefit.

scholarly journals Engineering a Decoy Substrate in Soybean to Enable Recognition of the Soybean Mosaic Virus NIa Protease

2019 ◽  
Vol 32 (6) ◽  
pp. 760-769 ◽  
Author(s):  
Matthew Helm ◽  
Mingsheng Qi ◽  
Shayan Sarkar ◽  
Haiyue Yu ◽  
Steven A. Whitham ◽  
...  
Keyword(s):  
Cell Death ◽  
Mosaic Virus ◽  
Pseudomonas Syringae ◽  
Cleavage Site ◽  
Soybean Mosaic Virus ◽  
Defense Responses ◽  
Cell Death Response ◽  
Arabidopsis Protein ◽  
Systemic Spread ◽  
Nia Protease

In Arabidopsis, recognition of the AvrPphB effector protease from Pseudomonas syringae is mediated by the disease resistance (R) protein RPS5, which is activated by AvrPphB-induced cleavage of the Arabidopsis protein kinase PBS1. The recognition specificity of RPS5 can be altered by substituting the AvrPphB cleavage site within PBS1 with cleavage sequences for other proteases, including proteases from viruses. AvrPphB also activates defense responses in soybean (Glycine max), suggesting that soybean may contain an R protein analogous to RPS5. It was unknown, however, whether this response is mediated by cleavage of a soybean PBS1-like protein. Here, we show that soybean contains three PBS1 orthologs and that their products are cleaved by AvrPphB. Further, transient expression of soybean PBS1 derivatives containing a five-alanine insertion at their AvrPphB cleavage sites activated cell death in soybean protoplasts, demonstrating that soybean likely contains an AvrPphB-specific resistance protein that is activated by a conformational change in soybean PBS1 proteins. Significantly, we show that a soybean PBS1 decoy protein modified to contain a cleavage site for the soybean mosaic virus (SMV) NIa protease triggers cell death in soybean protoplasts when cleaved by this protease, indicating that the PBS1 decoy approach will work in soybean, using endogenous PBS1 genes. Lastly, we show that activation of the AvrPphB-dependent cell death response effectively inhibits systemic spread of SMV in soybean. These data also indicate that decoy engineering may be feasible in other crop plant species that recognize AvrPphB protease activity.

scholarly journals In Spite of Induced Multiple Defense Responses, Tomato Plants Infected with Cucumber mosaic virus and D Satellite RNA Succumb to Systemic Necrosis

2003 ◽  
Vol 16 (6) ◽  
pp. 467-476 ◽  
Author(s):  
Ping Xu ◽  
Elison B. Blancaflor ◽  
Marilyn J. Roossinck
Keyword(s):  
Cucumber Mosaic Virus ◽  
Mosaic Virus ◽  
Expression Patterns ◽  
Defense Responses ◽  
Satellite Rna ◽  
Systemic Necrosis ◽  
Callose Deposition ◽  
Tomato Plants ◽  
Infected Tomato ◽  
Rna In Situ Hybridization

Cucumber mosaic virus (CMV) D satellite RNA (satRNA) attenuates the symptoms induced by CMV in most plants, but causes leaf epinasty and systemic necrosis in tomato plants, where programmed cell death (PCD) is involved. However, our understanding of the cellular and molecular responses to the infection of CMV D satRNA that result in this lethal disease remains limited. In this article, we show for the first time, by histochemical and molecular analysis, that multiple defense responses are specifically induced in CMV and D satRNA (CMV/D satRNA)-infected tomato plants but not in mock-inoculated or CMV-infected plants. These responses include callose deposition and hydrogen peroxide accumulation in infected plants. Furthermore, the transcription of several tomato defense-related genes (e.g., PR-1a1, PR-1b1, PR-2, and PR-10) were activated, and the expression of tomato PR-5 and some abiotic and biotic stress-responsive genes (e.g., catalase II and tomato analogs of Arabidopsis AtBI-1 and tobacco hsr203j) are enhanced. The activation and increase in expression of these genes is correlated with the appearance of leaf epinasty and the development of systemic necrosis in infected tomato plants, while increased expression of the hsr203j analog precedes the development of any disease symptoms. The spatial and temporal expression patterns of these genes as detected by RNA in situ hybridization point to the involvement of a complex developmental program that accompanies disease development resulting from CMV/D satRNA infection.

scholarly journals The P3 Protein of Turnip mosaic virus Can Alone Induce Hypersensitive Response-Like Cell Death in Arabidopsis thaliana Carrying TuNI

2010 ◽  
Vol 23 (2) ◽  
pp. 144-152 ◽  
Author(s):  
Bo Min Kim ◽  
Noriko Suehiro ◽  
Tomohide Natsuaki ◽  
Tsuyoshi Inukai ◽  
Chikara Masuta
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Death ◽  
Mosaic Virus ◽  
Dominant Gene ◽  
Gene Interaction ◽  
Hypersensitive Reaction ◽  
Turnip Mosaic Virus ◽  
Systemic Necrosis ◽  
Host Defense Response ◽  
Viral Factor

Strains TuR1 and TuC of Turnip mosaic virus (TuMV) induce different symptoms on Arabidopsis thaliana ecotype Landsberg erecta (Ler); plants infected with TuR1 develop systemic necrosis, while TuC causes mosaics. We previously found that the Ler systemic necrosis was controlled by a single dominant gene, TuNI (TuMV necrosis inducer), and that it was actually a form of host defense response leading to a hypersensitive reaction (HR)-like cell death. To identify the viral factor interacting with TuNI, the domain swapping between the genomic clones of TuR1 and TuC was carried out, and we identified the TuMV symptom determinant interacting with TuNI as the P3 gene. Moreover, it was found that the central 0.5-kb domain of P3, including three different amino acids between the two isolates, was responsible for the systemic HR. To verify that the P3 gene can alone induce necrosis, we analyzed the constitutive P3 expression in Ler transgenic plants and the transient P3 expression in Ler protoplasts. These results indicated that P3 alone caused HR-like cell death. In this study, we successfully demonstrated that the systemic necrosis by TuMV in Arabidopsis was determined by the gene-for-gene interaction between TuNI and P3 using the protoplast system for direct verification.

scholarly journals Engineering a decoy substrate in soybean to enable recognition of the Soybean Mosaic Virus NIa protease

2018 ◽  
Author(s):  
Matthew Helm ◽  
Mingsheng Qi ◽  
Shayan Sarkar ◽  
Haiyue Yu ◽  
Steven A. Whitham ◽  
...  
Keyword(s):  
Cell Death ◽  
Mosaic Virus ◽  
Pseudomonas Syringae ◽  
Cleavage Site ◽  
Soybean Mosaic Virus ◽  
Defense Responses ◽  
Cell Death Response ◽  
Arabidopsis Protein ◽  
Systemic Spread ◽  
Nia Protease

In Arabidopsis, recognition of the AvrPphB effector protease from Pseudomonas syringae is mediated by the disease resistance (R) protein RPS5, which is activated by AvrPphB-induced cleavage of the Arabidopsis protein kinase PBS1. The recognition specificity of RPS5 can be altered by substituting the AvrPphB cleavage site within PBS1 with cleavage sequences for other proteases, including proteases from viruses. AvrPphB also activates defense responses in soybean (Glycine max), suggesting that soybean may contain an R protein analogous to RPS5. It was unknown, however, whether this response is mediated by cleavage of a soybean PBS1-like protein. Here we show that soybean contains three PBS1 orthologs and that their products are cleaved by AvrPphB. Further, transient expression of soybean PBS1 derivatives containing a five-alanine insertion at their AvrPphB cleavage sites activated cell death in soybean protoplasts, demonstrating that soybean likely contains an AvrPphB-specific resistance protein that is activated by a conformational change in soybean PBS1 proteins. Significantly, we show that a soybean PBS1 decoy protein modified to contain a cleavage site for the Soybean mosaic virus (SMV) NIa protease triggers cell death in soybean protoplasts when cleaved by this protease, indicating that the PBS1 decoy approach will work in soybean using endogenous PBS1 genes. Lastly, we show that activation of the AvrPphB-dependent cell death response effectively inhibits systemic spread of SMV in soybean. These data also indicate that decoy engineering may be feasible in other crop plant species that recognize AvrPphB protease activity.

scholarly journals Barley stripe mosaic virus γb protein targets thioredoxin h-type 1 to dampen SA-mediated antiviral defenses

2022 ◽  
Author(s):  
Zhihao Jiang ◽  
Xuejiao Jin ◽  
Meng Yang ◽  
Qinglin Pi ◽  
Qing Cao ◽  
...  
Keyword(s):  
Mosaic Virus ◽  
Signaling Pathway ◽  
Reductase Activity ◽  
Defense Responses ◽  
Plant Viruses ◽  
Barley Stripe Mosaic Virus ◽  
Protein Targets ◽  
Thioredoxin H ◽  
Sa Signaling

Salicylic acid (SA) acts as a signaling molecule to perceive and defend against pathogen infections. Accordingly, pathogens evolve versatile strategies to disrupt the SA-mediated signal transduction. However, it is necessary to further characterize how plant viruses manipulate the SA-dependent defense responses. Here, we show that Barley stripe mosaic virus (BSMV) infection activates SA-mediated defense signaling pathway and upregulates the expression of Nicotiana benthamiana thioredoxin h-type 1 (NbTRXh1). The γb protein interacts directly with NbTRXh1 in vivo and in vitro. Overexpression of NbTRXh1, but not a reductase-defective mutant, impedes BSMV infection, whereas low NbTRXh1 expression level results in increased viral accumulation. Similar with its orthologues in Arabidopsis, NbTRXh1 also plays an essential role in SA signaling transduction in N. benthamiana. To counteract NbTRXh1-mediated defenses, the BSMV ?b protein targets NbTRXh1 to dampen its reductase activity and thereby impairing downstream SA defense genes expression to optimize viral cell-to-cell movement. We also found that NbTRXh1-mediated resistance defends against Lychnis ringspot virus, Beet black scorch virus, and Beet necrotic yellow vein virus. Taken together, our results reveal a novel role for the multifunctional γb protein in counteracting plant defense responses, and broadens the broad-spectrum antibiotic role of SA signaling pathway.

scholarly journals Optimizing the PBS1 Decoy System to Confer Resistance to Potyvirus Infection in Arabidopsis and Soybean

2020 ◽  
Vol 33 (7) ◽  
pp. 932-944 ◽  
Author(s):  
Sarah E. Pottinger ◽  
Aurelie Bak ◽  
Alexandra Margets ◽  
Matthew Helm ◽  
Lucas Tang ◽  
...  
Keyword(s):  
Cell Death ◽  
Plasma Membrane ◽  
Mosaic Virus ◽  
Pseudomonas Syringae ◽  
Soybean Mosaic Virus ◽  
Aphid Transmission ◽  
Defense Responses ◽  
Cell Death Response ◽  
Dependent Cell ◽  
Nia Protease

The Arabidopsis resistance protein RPS5 is activated by proteolytic cleavage of the protein kinase PBS1 by the Pseudomonas syringae effector protease AvrPphB. We have previously shown that replacing seven amino acids at the cleavage site of PBS1 with a motif cleaved by the NIa protease of turnip mosaic virus (TuMV) enables RPS5 activation upon TuMV infection. However, this engineered resistance conferred a trailing necrosis phenotype indicative of a cell-death response too slow to contain the virus. We theorized this could result from a positional mismatch within the cell between PBS1TuMV, RPS5, and the NIa protease. To test this, we relocalized PBS1TuMV and RPS5 to cellular sites of NIa accumulation. These experiments revealed that relocation of RPS5 away from the plasma membrane compromised RPS5-dependent cell death in Nicotiana benthamiana, even though PBS1 was efficiently cleaved. As an alternative approach, we tested whether overexpression of plasma membrane–localized PBS1TuMV could enhance RPS5 activation by TuMV. Significantly, overexpressing the PBS1TuMV decoy protein conferred complete resistance to TuMV when delivered by either agrobacterium or by aphid transmission, showing that RPS5-mediated defense responses are effective against bacterial and viral pathogens. Lastly, we have now extended this PBS1 decoy approach to soybean by modifying a soybean PBS1 ortholog to be cleaved by the NIa protease of soybean mosaic virus (SMV). Transgenic overexpression of this soybean PBS1 decoy conferred immunity to SMV, demonstrating that we can use endogenous PBS1 proteins in crop plants to engineer economically relevant disease resistant traits.

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