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.

scholarly journals Uncoupling Resistance from Cell Death in the Hypersensitive Response of Nicotiana Species to Cauliflower mosaic virus Infection

2001 ◽  
Vol 14 (1) ◽  
pp. 31-41 ◽  
Author(s):  
Anthony B. Cole ◽  
Lóránt Király ◽  
Kathleen Ross ◽  
James E. Schoelz
Keyword(s):  
Cell Death ◽  
Virus Infection ◽  
Mosaic Virus ◽  
Hypersensitive Response ◽  
Cauliflower Mosaic Virus ◽  
Resistance Response ◽  
Pr Protein ◽  
Pathogenesis Related ◽  
Lines Of Evidence ◽  
Mosaic Virus Infection

Cauliflower mosaic virus strain W260 elicits a hypersensitive response (HR) in leaves of Nicotiana edwardsonii, an interspecific hybrid derived from a cross between N. glutinosa and N. clevelandii. Interestingly, we found that N. glutinosa is resistant to W260, but responds with local chlorotic lesions rather than necrotic lesions. In contrast, N. clevelandii responds to W260 with systemic cell death. The reactions of the progenitors of N. edwardsonii to W260 infection indicated that each contributed a factor toward the development of HR. In this study, we present two lines of evidence to show that the resistance and cell death that comprise the HR elicited by W260 can indeed be uncoupled. First, we showed that the non-necrotic resistance response of N. glutinosa could be converted to HR when these plants were crossed with N. clevelandii. Second, we found that cell death and resistance segregated independently in the F2 population of a cross between N. edwardsonii and N. clevelandii. We concluded that the resistance of N. edwardsonii to W260 infection was conditioned by a gene derived from N. glutinosa, whereas cell death was conditioned by a gene derived from N. clevelandii. An analysis of pathogenesis-related (PR) protein expression in response to W260 infection revealed that elicitation of PR proteins was associated with resistance rather than with the onset of cell death.

scholarly journals Agroinfiltration of Cauliflower mosaic virus Gene VI Elicits Hypersensitive Response in Nicotiana Species

2000 ◽  
Vol 13 (11) ◽  
pp. 1275-1279 ◽  
Author(s):  
Karuppaiah Palanichelvam ◽  
Anthony B. Cole ◽  
Monir Shababi ◽  
James E. Schoelz
Keyword(s):  
Cell Death ◽  
Agrobacterium Tumefaciens ◽  
Mosaic Virus ◽  
Virus Strain ◽  
Hypersensitive Response ◽  
Frameshift Mutation ◽  
Binary Vector ◽  
Cauliflower Mosaic Virus ◽  
Host Defenses ◽  
Nicotiana Species

Cauliflower mosaic virus strain W260 induces hypersensitive response (HR) in Nicotiana edwardsonii and systemic cell death in N. clevelandii. In contrast, the D4 strain of Cauliflower mosaic virus evades the host defenses in Nicotiana species; it induces chlorotic primary lesions and a systemic mosaic in both hosts. Previous studies with chimeric viruses had indicated that gene VI of W260 was responsible for elicitation of HR or cell death. To prove conclusively that W260 gene VI is responsible, we inserted gene VI of W260 and D4 into the Agrobacterium tumefaciens binary vector pKYLX7. Agroinfiltration of these constructs into the leaves of N. edwardsonii and N. clevelandii revealed that gene VI of W260 elicited HR in N. edwardsonii 4 to 5 days after infiltration and cell death in N. clevelandii approximately 9 to 12 days after infiltration. In contrast, gene VI of D4 did not elicit HR or cell death in either Nicotiana species. A frameshift mutation introduced into gene VI of W260 abolished its ability to elicit HR or cell death in both Nicotiana species, demonstrating that the elicitor is the gene VI protein.

scholarly journals Extreme Resistance to Viruses in Potato and Soybean

2021 ◽  
Vol 12 ◽  
Author(s):  
Brian T. Ross ◽  
Nina K. Zidack ◽  
Michelle L. Flenniken
Keyword(s):  
Cell Death ◽  
Potato Virus ◽  
Hypersensitive Response ◽  
Plant Pathogens ◽  
Molecular Mechanisms ◽  
Soybean Mosaic Virus ◽  
Plant Viruses ◽  
Infection Site ◽  
Extreme Resistance ◽  
Resistance To Viruses

Plant pathogens, including viruses, negatively impact global crop production. Plants have evolved complex immune responses to pathogens. These responses are often controlled by nucleotide-binding leucine-rich repeat proteins (NLRs), which recognize intracellular, pathogen-derived proteins. Genetic resistance to plant viruses is often phenotypically characterized by programmed cell death at or near the infection site; a reaction termed the hypersensitive response. Although visualization of the hypersensitive response is often used as a hallmark of resistance, the molecular mechanisms leading to the hypersensitive response and associated cell death vary. Plants with extreme resistance to viruses rarely exhibit symptoms and have little to no detectable virus replication or spread beyond the infection site. Both extreme resistance and the hypersensitive response can be activated by the same NLR genes. In many cases, genes that normally provide an extreme resistance phenotype can be stimulated to cause a hypersensitive response by experimentally increasing cellular levels of pathogen-derived elicitor protein(s). The molecular mechanisms of extreme resistance and its relationship to the hypersensitive response are largely uncharacterized. Studies on potato and soybean cultivars that are resistant to strains of Potato virus Y (PVY), Potato virus X (PVX), and Soybean mosaic virus (SMV) indicate that abscisic acid (ABA)-mediated signaling and NLR nuclear translocation are important for the extreme resistance response. Recent research also indicates that some of the same proteins are involved in both extreme resistance and the hypersensitive response. Herein, we review and synthesize published studies on extreme resistance in potato and soybean, and describe studies in additional species, including model plant species, to highlight future research avenues that may bridge the gaps in our knowledge of plant antiviral defense mechanisms.

scholarly journals Systemic Cell Death Is Elicited by the Interaction of a Single Gene in Nicotiana clevelandii and Gene VI of Cauliflower Mosaic Virus

1999 ◽  
Vol 12 (10) ◽  
pp. 919-925 ◽  
Author(s):  
Lóránt Király ◽  
Anthony B. Cole ◽  
June E. Bourque ◽  
James E. Schoelz
Keyword(s):  
Cell Death ◽  
Mosaic Virus ◽  
Hypersensitive Response ◽  
Single Gene ◽  
Cauliflower Mosaic Virus ◽  
Host Gene ◽  
Mosaic Symptom ◽  
Single Host ◽  
Cell Death Gene ◽  
Nicotiana Clevelandii

Cauliflower mosaic virus (CaMV) strains D4 and W260 can be distinguished by the type of symptoms they induce in Nicotiana clevelandii and N. edwardsonii. W260 induces systemic cell death in addition to a mosaic symptom in N. clevelandii and a hypersensitive response (HR) in N. edwardsonii, whereas D4 induces a systemic mosaic in both hosts. To determine which W260 genes are responsible for systemic cell death, chimeric viruses were constructed between the D4 and W260 strains. It was found that W260 gene VI was responsible for the elicitation of systemic cell death; previous studies had shown that this same gene elicited HR in N. edwardsonii. An immunological analysis of plants infected with W260 or D4 indicated that the systemic cell death symptom was not associated with enhanced levels of either W260 virions or the W260 gene VI product. To investigate the inheritance of systemic cell death, crosses were made between N. clevelandii and N. bigelovii, a host that reacts with a systemic mosaic symptom upon infection with W260. All F1 plants developed a systemic mosaic after inoculation with W260, whereas the F2 generation segregated 3:1 for systemic mosaic versus cell death. The plant gene responsible for cell death was designated ccd1, for CaMV cell death gene. These results demonstrate that the systemic cell death symptom in N. clevelandii is induced by the interaction between a single host gene and gene VI of CaMV.

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.

New threats to endangered Cook’s scurvy grass (Lepidium oleraceum; Brassicaceae): introduced crop viruses and the extent of their spread

2013 ◽  
Vol 61 (2) ◽  
pp. 161 ◽  
Author(s):  
Josh C. C. M. Van Vianen ◽  
Gary J. Houliston ◽  
John D. Fletcher ◽  
Peter B. Heenan ◽  
Hazel M. Chapman
Keyword(s):  
Mosaic Virus ◽  
Natural Populations ◽  
First Record ◽  
Plant Viruses ◽  
Cauliflower Mosaic Virus ◽  
Economic Output ◽  
Threatened Plant Species ◽  
High Incidence ◽  
Turnip Yellows Virus ◽  
Coastal Plant

To date, most research conducted on plant viruses has centred on agricultural systems where viruses greatly reduce economic output. Introduced viruses are globally common and there is a lack of knowledge around how they might affect natural populations. Although it has been suggested that infectious disease may have played an underestimated role in past species extinctions, there is little empirical evidence. Cook’s scurvy grass (Lepidium oleraceum Sparrm. ex G.Forst; Brassicaceae) is a threatened coastal plant endemic to New Zealand. Following the discovery of Turnip mosaic virus (TuMV) in some glasshouse cultivated specimens, we surveyed wild extant Lepidium populations on the Otago coast for TuMV while screening for two other common crop viruses. We show that TuMV is almost ubiquitous among remaining wild L. oleraceum populations on the South Island’s east coast and report the first record of L. oleraceum as a host for both Cauliflower mosaic virus and Turnip yellows virus. The high incidence of virus infection throughout the study populations may make this system one of the first examples of introduced viruses affecting the conservation of a threatened plant species.

scholarly journals A Single Amino Acid Position in the Helper Component of Cauliflower Mosaic Virus Can Change the Spectrum of Transmitting Vector Species

2005 ◽  
Vol 79 (21) ◽  
pp. 13587-13593 ◽  
Author(s):  
Aranzazu Moreno ◽  
Eugénie Hébrard ◽  
Marilyne Uzest ◽  
Stéphane Blanc ◽  
Alberto Fereres
Keyword(s):  
Amino Acid ◽  
Mosaic Virus ◽  
Amino Acid Position ◽  
Plant Viruses ◽  
Aphid Species ◽  
Virus Vector ◽  
Cauliflower Mosaic Virus ◽  
Vector Species ◽  
Helper Component ◽  
Mode Of Transmission

ABSTRACT Viruses frequently use insect vectors to effect rapid spread through host populations. In plant viruses, vector transmission is the major mode of transmission, used by nearly 80% of species described to date. Despite the importance of this phenomenon in epidemiology, the specificity of the virus-vector relationship is poorly understood at both the molecular and the evolutionary level, and very limited data are available on the precise viral protein motifs that control specificity. Here, using the aphid-transmitted Cauliflower mosaic virus (CaMV) as a biological model, we confirm that the “noncirculative” mode of transmission dominant in plant viruses (designated “mechanical vector transmission” in animal viruses) involves extremely specific virus-vector recognition, and we identify an amino acid position in the “helper component” (HC) protein of CaMV involved in such recognition. Site-directed mutagenesis revealed that changing the residue at this position can differentially affect transmission rates obtained with various aphid species, thus modifying the spectrum of vector species for CaMV. Most interestingly, in a virus line transmitted by a single vector species, we observed the rapid appearance of a spontaneous mutant specifically losing its transmissibility by another aphid species. Hence, in addition to the first identification of an HC motif directly involved in specific vector recognition, we demonstrate that change of a virus to a different vector species requires only a single mutation and can occur rapidly and spontaneously.

Nuclear targeting of the cauliflower mosaic virus (CaMV) genomeThis review is one of a selection of papers published in the Special Issue on Plant Cell Biology.

2006 ◽  
Vol 84 (4) ◽  
pp. 565-571
Author(s):  
Julie Champagne ◽  
Denis Leclerc
Keyword(s):  
Mosaic Virus ◽  
Nuclear Localization ◽  
Nuclear Localization Signal ◽  
Cell Biology ◽  
Plant Viruses ◽  
Cauliflower Mosaic Virus ◽  
Nuclear Pore ◽  
Regulatory Sequences ◽  
Nuclear Targeting ◽  
Localization Signal

The delivery of the double-stranded DNA viral genome into the nucleus is a critical step for the type member of Caulimoviridae, cauliflower mosaic virus (CaMV). The nucleocapsid (NC) of CaMV is directly involved in this process. A nuclear localization signal located at the N-terminus of the NC was shown to be exposed at the surface of the virion. This nuclear localization signal appears to be important to direct the virus to the nuclear pore complex. The nuclear targeting of the NC needs to be tightly regulated because the process of virus assembly, which also involves the viral NC, occurs in the cytosol. It is now accepted that the N- and C-terminal extensions of the viral NC precursor are efficient regulatory sequences that determine the localization of the viral NC in infected leaves. Proteolytic maturation and phosphorylation of the N- and C-terminal extensions are also important in the regulation of this process. Despite these recent discoveries, the transport of CaMV toward and into the nucleus during early events in the infection cycle remains unclear. In this review, we summarize recent advances that explain the mechanisms of targeting of the CaMV genome to the nucleus and extract from other related animal and plant viruses mechanisms that could hint at the possible strategies used by CaMV to enter the nucleus.

scholarly journals The secreted hypersensitive response inducing protein 1 fromBotrytis cinereadisplays non-canonical PAMP-activity

2020 ◽  
Author(s):  
Tanja Jeblick ◽  
Thomas Leisen ◽  
Christina E. Steidele ◽  
Jonas Müller ◽  
Florian Mahler ◽  
...  
Keyword(s):  
Cell Death ◽  
Plant Cell ◽  
Hypersensitive Response ◽  
Plant Pathogens ◽  
Infection Process ◽  
Host Cells ◽  
Plant Responses ◽  
Cell Wall Degrading Enzymes ◽  
Molecular Pattern ◽  
Biotrophic Pathogens

AbstractAccording to their lifestyle, plant pathogens are divided into biotrophic and necrotrophic organisms. While biotrophic pathogens establish a relationship with living host cells, necrotrophic pathogens rapidly kill host cells and feed on the cell debris. To this end, the necrotrophic ascomycete fungusBotrytis cinereasecretes large amounts of phytotoxic proteins and cell wall degrading enzymes. However, the precise role of these proteins during the infection process is unknown. Here we report on the identification and characterization of the previously unknown toxic protein hypersensitive response inducing protein 1 (Hip1), which induces plant cell death. We found the adoption of a folded protein structure to be a prerequisite for Hip1 to exert its necrosis-inducing activity inNicotiana benthamiana. Localization and the induction of specific plant responses by Hip1 indicate recognition as pathogen-associated molecular pattern at the plant plasma membrane. Our results demonstrate that recognition of Hip1, even in the absence of obvious enzymatic or poreforming activity, induces strong plant defense reactions eventually leading to plant cell death.

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