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Simon Santa Cruz - One of the best experts on this subject based on the ideXlab platform.
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analysis of the n gene Hypersensitive Response induced by a fluorescently tagged tobacco mosaic virus
Plant Physiology, 2000Co-Authors: Kathryn M Wright, George H Duncan, Katja S Pradel, Fiona Carr, Susannah Wood, Karl J Oparka, Simon Santa CruzAbstract:The Hypersensitive Response (HR) triggered on Nicotiana edwardsonii by tobacco mosaic virus was studied using a modified viral genome that directed expression of the green fluorescent protein. Inoculated plants were initially incubated at 32°C to inhibit the N gene-mediated HR. Transfer to 20°C initiated the HR, and fluorescent infection foci were monitored for early HR-associated events. Membrane damage, which preceded visible cell collapse by more than 3 h, was accompanied by a transient restriction of the xylem within infection sites. Following cell collapse and the rapid desiccation of tissue undergoing the HR, isolated, infected cells were detected at the margin of necrotic lesions. These virus-infected cells were able to reinitiate infection on transfer to 32°C, however, if maintained at 20°C they eventually died. The results indicate that the tobacco mosaic virus-induced HR is a two-phase process with an early stage culminating in rapid cell collapse and tissue desiccation followed by a more extended period during which the remaining infected cells are eliminated.
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bax induced cell death in tobacco is similar to the Hypersensitive Response
Proceedings of the National Academy of Sciences of the United States of America, 1999Co-Authors: Christophe Lacomme, Simon Santa CruzAbstract:Bax, a death-promoting member of the Bcl-2 family of proteins, triggered cell death when expressed in plants from a tobacco mosaic virus vector. Analysis of Bax deletion mutants demonstrated a requirement for the BH1 and BH3 domains in promoting rapid cell death, whereas deletion of the carboxyl-terminal transmembrane domain completely abolished the lethality of Bax in plants. The phenotype of cell death induced by Bax closely resembled the Hypersensitive Response induced by wild-type tobacco mosaic virus in tobacco plants carrying the N gene. The cell death-promoting function of Bax in plants correlated with accumulation of the defense-related protein PR1, suggesting Bax activated an endogenous cell-death program in plants. In support of this view, both N gene- and Bax-mediated cell death was blocked by okadaic acid, an inhibitor of protein phosphatase activity. The ability of Bax to induce cell death and a defense reaction in plants suggests that some features of animal and plant cell death processes may be shared.
Carl H. Mesarich - One of the best experts on this subject based on the ideXlab platform.
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Specific Hypersensitive Response–Associated Recognition of New Apoplastic Effectors from Cladosporium fulvum in Wild Tomato
Molecular Plant-Microbe Interactions, 2018Co-Authors: Carl H. Mesarich, Hanna Rovenich, Scott A. Griffiths, Changchun Wang, Mansoor Karimi Jashni, Aleksandar Mihajlovski, Jérôme Collemare, Lukas Hunziker, Cecilia H. Deng, Ate Van Der BurgtAbstract:Tomato leaf mold disease is caused by the biotrophic fungus Cladosporium fulvum. During infection, C. fulvum produces extracellular small secreted protein (SSP) effectors that function to promote colonization of the leaf apoplast. Resistance to the disease is governed by Cf immune receptor genes that encode receptor-like proteins (RLPs). These RLPs recognize specific SSP effectors to initiate a Hypersensitive Response (HR) that renders the pathogen avirulent. C. fulvum strains capable of overcoming one or more of all cloned Cf genes have now emerged. To combat these strains, new Cf genes are required. An effectoromics approach was employed to identify wild tomato accessions carrying new Cf genes. Proteomics and transcriptome sequencing were first used to identify 70 apoplastic in planta-induced C. fulvum SSPs. Based on sequence homology, 61 of these SSPs were novel or lacked known functional domains. Seven, however, had predicted structural homology to antimicrobial proteins, suggesting a possible role in mediating antagonistic microbe-microbe interactions in planta. Wild tomato accessions were then screened for HR-associated recognition of 41 SSPs, using the Potato virus X-based transient expression system. Nine SSPs were recognized by one or more accessions, suggesting that these plants carry new Cf genes available for incorporation into cultivated tomato.
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specific Hypersensitive Response associated recognition of new apoplastic effectors from cladosporium fulvum in wild tomato
Molecular Plant-microbe Interactions, 2018Co-Authors: Carl H. Mesarich, Hanna Rovenich, Scott A. Griffiths, Changchun Wang, Aleksandar Mihajlovski, Bilal ӧkmen, Mansoor Karimi Jashni, Jérôme CollemareAbstract:Tomato leaf mold disease is caused by the biotrophic fungus Cladosporium fulvum. During infection, C. fulvum produces extracellular small secreted protein (SSP) effectors that function to promote colonization of the leaf apoplast. Resistance to the disease is governed by Cf immune receptor genes that encode receptor-like proteins (RLPs). These RLPs recognize specific SSP effectors to initiate a Hypersensitive Response (HR) that renders the pathogen avirulent. C. fulvum strains capable of overcoming one or more of all cloned Cf genes have now emerged. To combat these strains, new Cf genes are required. An effectoromics approach was employed to identify wild tomato accessions carrying new Cf genes. Proteomics and transcriptome sequencing were first used to identify 70 apoplastic in planta-induced C. fulvum SSPs. Based on sequence homology, 61 of these SSPs were novel or lacked known functional domains. Seven, however, had predicted structural homology to antimicrobial proteins, suggesting a possible role in mediating antagonistic microbe-microbe interactions in planta. Wild tomato accessions were then screened for HR-associated recognition of 41 SSPs, using the Potato virus X-based transient expression system. Nine SSPs were recognized by one or more accessions, suggesting that these plants carry new Cf genes available for incorporation into cultivated tomato.
Luis A. J. Mur - One of the best experts on this subject based on the ideXlab platform.
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Nitrite and nitric oxide are important in the adjustment of primary metabolism during the Hypersensitive Response in tobacco
Journal of experimental botany, 2019Co-Authors: Luis A. J. Mur, Aprajita Kumari, Frans J. M. Harren, Yariv Brotman, Jürgen Zeier, Julien Mandon, Simona M. Cristescu, Werner M. Kaiser, Alisdair R. Fernie, Kapuganti Jagadis GuptaAbstract:Nitrate and ammonia deferentially modulate primary metabolism during the Hypersensitive Response in tobacco. In this study, tobacco RNAi lines with low nitrite reductase (NiRr) levels were used to investigate the roles of nitrite and nitric oxide (NO) in this process. The lines accumulate NO2-, with increased NO generation, but allow sufficient reduction to NH4+ to maintain plant viability. For wild-type (WT) and NiRr plants grown with NO3-, inoculation with the non-host biotrophic pathogen Pseudomonas syringae pv. phaseolicola induced an accumulation of nitrite and NO, together with a Hypersensitive Response (HR) that resulted in decreased bacterial growth, increased electrolyte leakage, and enhanced pathogen resistance gene expression. These Responses were greater with increases in NO or NO2- levels in NiRr plants than in the WT under NO3- nutrition. In contrast, WT and NiRr plants grown with NH4+ exhibited compromised resistance. A metabolomic analysis detected 141 metabolites whose abundance was differentially changed as a result of exposure to the pathogen and in Response to accumulation of NO or NO2-. Of these, 13 were involved in primary metabolism and most were linked to amino acid and energy metabolism. HR-associated changes in metabolism that are often linked with primary nitrate assimilation may therefore be influenced by nitrite and NO production.
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accumulation of chlorophyll catabolites photosensitizes the Hypersensitive Response elicited by pseudomonas syringae in arabidopsis
New Phytologist, 2010Co-Authors: Luis A. J. Mur, Sylvain Aubry, Madhav Mondhe, Alison H Kingstonsmith, J Gallagher, Emma Timmstaravella, C L James, Istvan Papp, Stefan Hortensteiner, Howard ThomasAbstract:• The staygreen (SGR) gene encodes a chloroplast-targeted protein which promotes chlorophyll degradation via disruption of light-harvesting complexes (LHCs). • Over-expression of SGR in Arabidopsis (SGR-OX) in a Columbia-0 (Col-0) background caused spontaneous necrotic flecking. To relate this to the Hypersensitive Response (HR), Col-0, SGR-OX and RNAi SGR (SGRi) lines were challenged with Pseudomonas syringae pv tomato (Pst) encoding the avirulence gene avrRpm1. Increased and decreased SGR expression, respectively, accelerated and suppressed the kinetics of HR-cell death. In Col-0, SGR transcript increased at 6 h after inoculation (hai) when tissue electrolyte leakage indicated the initiation of cell death. • Excitation of the chlorophyll catabolite pheophorbide (Pheide) leads to the formation of toxic singlet oxygen ((1)O(2)). Pheide was first detected at 6 hai with Pst avrRpm1 and was linked to (1)O(2) generation and correlated with reduced Pheide a oxygenase (PaO) protein concentrations. The maximum quantum efficiency of photosystem II (F(v)/F(m)), quantum yield of electron transfer at photosystem II (φPSII), and photochemical quenching (qP) decreased at 6 hai in Col-0 but not in SGRi. Disruption of photosynthetic electron flow will cause light-dependent H(2)O(2) generation at 6 hai. • We conclude that disruption of LHCs, possibly influenced by SGR, and absence of PaO produce phototoxic chlorophyll catabolites and oxidative stress leading to the HR.
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the Hypersensitive Response the centenary is upon us but how much do we know
Journal of Experimental Botany, 2008Co-Authors: Luis A. J. Mur, Paul Kenton, Amanda J Lloyd, Helen J Ougham, Elena PratsAbstract:With the centenary of the first descriptions of ‘Hypersensitiveness’ following pathogenic challenge upon us, it is appropriate to assess our current understanding of the Hypersensitive Response (HR) form of cell death. In recent decades our understanding of the initiation, associated signalling, and some important proteolytic events linked to the HR has dramatically increased. Genetic approaches are increasingly elucidating the function of the HR initiating resistance genes and there have been extensive analyses of death-associated signals, calcium, reactive oxygen species (ROS), nitric oxide, salicylic acid, and now sphingolipids. At the same time, attempts to draw parallels between mammalian apoptosis and the HR have been largely unsuccessful and it may be better to consider the HR to be a distinctive form of plant cell death. We will consider if the HR form of cell death may occur through metabolic dysfunction in which malfunctioning organelles may play a major role. This review will highlight that although our knowledge of parts of the HR is excellent, a comprehensive molecular model is still to be attained.
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eLS - Hypersensitive Response in Plants
Encyclopedia of Life Sciences, 2007Co-Authors: Luis A. J. MurAbstract:The Hypersensitive Response (HR) in plants is a rapid and highly localized cell death that may be evoked by pathogen challenge. The HR is not a disease syndrome but is an effective, host-regulated defence Response which contributes towards the neutralization of the invading pathogen. Research into the elicitation and elaboration of the HR is a major research theme in plant biology where there is a close interaction between laboratory-based experimental science and plant breeders in order to generate pathogen-resistant crops. Keywords: Hypersensitive Response; programmed cell death; pathogen; resistance; gene-for-gene
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NO provides mainly avr-dependent inputs into cell death mechanisms associated with the Hypersensitive Response in tobacco
Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology, 2007Co-Authors: Luis A. J. Mur, Paul Kenton, Luc-jan Laarhoven, Frans J. M. Harren, Aileen R. SmithAbstract:Mur, L. A. J., Kenton, P., Harren, F., Laarhoven, L., Smith, A. (2007). NO provides mainly avr-dependent inputs into cell death mechanisms associated with the Hypersensitive Response in tobacco. Comparative Biochemistry and Physiology A - Molecular & Integrative Physiology, 146, (4), Supplement 1, S256. Abstracts of the Annual Main Meeting of the Society for Experimental Biology, Glasgow, Scotland, 31st March-4th April, 2007.
H S Shetty - One of the best experts on this subject based on the ideXlab platform.
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Hypersensitive Response, cell death and histochemical localisation of hydrogen peroxide in host and non‐host seedlings infected with the downy mildew pathogen Sclerospora graminicola
Annals of Applied Biology, 2001Co-Authors: B.s. Kumudini, N S Vasanthi, H S ShettyAbstract:Hypersensitive Response, cell death and release of hydrogen peroxide as measures of host and non-host defense mechanisms upon inoculation with the downy mildew pathogen Sclerospora graminicola were studied histochemically at the light microscopy level. The materials consisted of coleoptile tissues of the highly susceptible (cv. HB3), highly resistant (cv. IP18293) and induced resistant pearl millet host seedlings and non-host sorghum (cv. SGMN 10/8) and cotyledon of french bean (cv. S9). Resistance up to 80% protection against the downy mildew pathogen was induced in the highly susceptible HB3 cultivar of pearl millet by treating the seeds with 2% aqueous leaf extract of Datura metel for 3 h. Time course study with the pathogen inoculated highly resistant pearl millet cultivar revealed the appearance of Hypersensitive Response in 20% of seedlings as necrotic spots as early as 2 h after inoculation. In contrast, a similar reaction was observed in the highly susceptible pearl millet cultivar only 8 h after inoculation with the pathogen. In induced resistant seedlings, appearance of Hypersensitive Response was recorded 4 h after inoculation. Delayed Hypersensitive Response was observed in both the non-host species at 10 h after inoculation. Hypersensitive Response in the seedlings of the highly resistant pearl millet cultivar 24 h after inoculation showed 100% Hypersensitive Response, which was not observed in susceptible and non-host species, although the induced resistant seedlings showed 90% Hypersensitive Response after that period of time. Cell death in the tissues of the test seedlings was also observed to change with time. Statistical analysis revealed that the tissues of highly resistant pearl millet seedlings required 2.9 h to attain 50% cell death. Tissues of induced resistant and highly susceptible pearl millet seedlings required 4.65 and 6.50 h respectively. In non-hosts, 50% cell death was not recorded. Quantification of hydrogen peroxide in the tissue periplasmic spaces of the test seedlings revealed 2.94 h as the time required for 50% hydrogen peroxide accumulation in the tissues of highly resistant pearl millet seedlings. Tissues of induced resistant and highly susceptible pearl millet seedlings needed 3.76 and 5.5 h respectively. Fifty percent hydrogen peroxide localisation in non-hosts could not be recorded. These results suggested the involvement of hydrogen peroxide, cell death and Hypersensitive Response in pearl millet host defense against S. graminicola.
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Hypersensitive Response cell death and histochemical localisation of hydrogen peroxide in host and non host seedlings infected with the downy mildew pathogen sclerospora graminicola
Annals of Applied Biology, 2001Co-Authors: B.s. Kumudini, N S Vasanthi, H S ShettyAbstract:Hypersensitive Response, cell death and release of hydrogen peroxide as measures of host and non-host defense mechanisms upon inoculation with the downy mildew pathogen Sclerospora graminicola were studied histochemically at the light microscopy level. The materials consisted of coleoptile tissues of the highly susceptible (cv. HB3), highly resistant (cv. IP18293) and induced resistant pearl millet host seedlings and non-host sorghum (cv. SGMN 10/8) and cotyledon of french bean (cv. S9). Resistance up to 80% protection against the downy mildew pathogen was induced in the highly susceptible HB3 cultivar of pearl millet by treating the seeds with 2% aqueous leaf extract of Datura metel for 3 h. Time course study with the pathogen inoculated highly resistant pearl millet cultivar revealed the appearance of Hypersensitive Response in 20% of seedlings as necrotic spots as early as 2 h after inoculation. In contrast, a similar reaction was observed in the highly susceptible pearl millet cultivar only 8 h after inoculation with the pathogen. In induced resistant seedlings, appearance of Hypersensitive Response was recorded 4 h after inoculation. Delayed Hypersensitive Response was observed in both the non-host species at 10 h after inoculation. Hypersensitive Response in the seedlings of the highly resistant pearl millet cultivar 24 h after inoculation showed 100% Hypersensitive Response, which was not observed in susceptible and non-host species, although the induced resistant seedlings showed 90% Hypersensitive Response after that period of time. Cell death in the tissues of the test seedlings was also observed to change with time. Statistical analysis revealed that the tissues of highly resistant pearl millet seedlings required 2.9 h to attain 50% cell death. Tissues of induced resistant and highly susceptible pearl millet seedlings required 4.65 and 6.50 h respectively. In non-hosts, 50% cell death was not recorded. Quantification of hydrogen peroxide in the tissue periplasmic spaces of the test seedlings revealed 2.94 h as the time required for 50% hydrogen peroxide accumulation in the tissues of highly resistant pearl millet seedlings. Tissues of induced resistant and highly susceptible pearl millet seedlings needed 3.76 and 5.5 h respectively. Fifty percent hydrogen peroxide localisation in non-hosts could not be recorded. These results suggested the involvement of hydrogen peroxide, cell death and Hypersensitive Response in pearl millet host defense against S. graminicola.
Eric Lam - One of the best experts on this subject based on the ideXlab platform.
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Programmed cell death, mitochondria and the plant Hypersensitive Response
Nature, 2001Co-Authors: Eric Lam, Naohiro Kato, Michael T. LawtonAbstract:The plant Response to attempted infection by microbial pathogens is often accompanied by rapid cell death in and around the initial infection site, a reaction known as the Hypersensitive Response. This Response is associated with restricted pathogen growth and represents a form of programmed cell death (PCD). Recent pharmacological and molecular studies have provided functional evidence for the conservation of some of the basic regulatory mechanisms underlying the Response to pathogens and the activation of PCD in animal and plant systems. In animals, the mitochondrion integrates diverse cellular stress signals and initiates the death execution pathway, and studies indicate a similar involvement for mitochondria in regulating PCD in plants. But many of the cell-death regulators that have been characterized in humans, worms and flies are absent from the Arabidopsis genome, indicating that plants probably use other regulators to control this process.
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BAXing in the Hypersensitive Response.
Trends in plant science, 1999Co-Authors: Eric Lam, Olga Del Pozo, Dominique PontierAbstract:Most of the cell death pathways that have been characterized in animal systems require caspase activation as a deterministic step. In some cases, this might involve mitochondria participation, whereas others by-pass this organelle and activate caspases using protein–protein interactions. In organisms such as C. elegans, where a simpler set of cell death regulators is known, no evidence for cytochrome c involvement has been found. Thus, this particular mode of cell death activation might be augmented by other types of pathways that bypass mitochondrial involvement in the activation of cell death. The conserved ability of Bax to activate cell death in yeast and plants via its interaction with the mitochondrial membrane is consistent with the view that this organelle can serve as a cell death activator in many eukaryotes. However, the precise details of why Bax localization to these mitochondria leads to cell death remains to be elucidated. A mammalian gene, Bax Inhibitor 1 (BI-1), has been isolated on the basis of its ability to repress Bax-induced yeast cell death15xBax inhibitor-1, a mammalian apoptosis suppressor identified by functional screening in yeast. Xu, Q. and Reed, J.C. Mol. Cell. 1998; 1: 337–346Abstract | Full Text | Full Text PDF | PubMedSee all References15. When overexpressed in mammalian cells, cell death induction by several different agents and treatments is suppressed by BI-1, with the exception of Fas-induced cell death, which does not involve mitochondrial participation. Interestingly, possible BI-1 homologs have been found in the Arabidopsis and C. elegans sequence databases, although their homologies to mammalian BI-1 homologs are rather low (29% and 21% identity, respectively). It will be interesting to determine whether mammalian and Arabidopsis BI-1 are able to suppress Bax- induced cell death in plants as well as Hypersensitive Response cell death. Another key experiment would be to examine whether cytochrome c release into the cytosol is used by plants to activate cell-death-processes, such as the Hypersensitive Response. This might link the possible participation of plant mitochondria in Hypersensitive Response cell death10xBax-induced cell death in tobacco is similar to the Hypersensitive Response. Lacomme, C. and Santa Cruz, S. Proc. Natl. Acad. Sci. U. S. A. 1999; 96: 7956–7961CrossRef | PubMed | Scopus (220)See all References10 to observations that caspase-like protease activity is activated and appears to be necessary for the Hypersensitive Response13xCaspases and programmed cell death in the Hypersensitive Response of plants to pathogens. del Pozo, O. and Lam, E. Curr. Biol. 1998; 8: 1129–1132Abstract | Full Text | Full Text PDF | PubMedSee all References13.
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Markers for Hypersensitive Response and senescence show distinct patterns of expression.
Plant molecular biology, 1999Co-Authors: Dominique Pontier, Susheng Gan, Richard M. Amasino, Dominique Roby, Eric LamAbstract:Controlled cellular suicide is an important process that can be observed in various organs during plant development. From the generation of proper sexual organs in monoecious plants to the Hypersensitive Response (HR) that occurs during incompatible pathogen interactions, programmed cell death (PCD) can be readily observed. Although several biochemical and morphological parameters have been described for various types of cell death in plants, the relationships existing between those different types of PCD events remain unclear. In this work, we set out to examine if two early molecular markers of HR cell death (HIN1 and HSR203J) as well as a senescence marker (SAG12) are coordinately induced during these processes. Our result indicates that although there is evidence of some cross-talk between both cell death pathways, spatial and temporal characteristics of activation for these markers during Hypersensitive Response and senescence are distinct. These observations indicate that these markers are relatively specific for different cell death programs. Interestingly, they also revealed that a senescence-like process seems to be triggered at the periphery of the HR necrotic lesion. This suggests that cells committed to die during the HR might release a signal able to induce senescence in the neighboring cells. This phenomenon could correspond to the establishment of a second barrier against pathogens. Lastly, we used those cell death markers to better characterize cell death induced by copper and we showed that this abiotic induced cell death presents similarities with HR cell death.
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Caspases and programmed cell death in the Hypersensitive Response of plants to pathogens
Current Biology, 1998Co-Authors: Olga Del Pozo, Eric LamAbstract:The Hypersensitive Response (HR) is induced by certain plant pathogens and involves programmed cell death (PCD) to restrict the spread of pathogens from the infection site [1]. Concurrent with the induction of cell death, the host activates a defense Response [2]. The cell death associated with the HR in several plant-pathogen systems has morphological similarities to animal apoptosis [3,4], which suggests that cell death mechanisms in plants and animals may share common components that lead to similar cellular events. Caspases are conserved cysteine proteases that regulate animal PCD [5]; caspase activity or an involvement of caspases in cell death has yet to be reported in plants. In this work, we investigated the participation of caspases in HR cell death. Caspase-specific peptide inhibitors, Ac-YVAD-CMK [6] and Ac-DEVD-CHO [7], could abolish bacteria-induced plant PCD but did not significantly affect the induction of other aspects of HR, such as the expression of defense genes. This result confirmed our previous model that cell death can be uncoupled from defense gene activation during HR [8]. Caspase-like proteolytic activity was detected in tobacco tissues that were developing HR following infection with tobacco mosaic virus (TMV). Our results provide evidence for the presence of caspase-like plant protease(s) that participate in HR cell death.