Symptomless Resistant Response Instead of the Hypersensitive Reaction in Tobacco Leaves after Infiltration of Heterologous Pathovars of Pseudomonas syringae

Klement, Z.; Bozsó, Zoltán; Ott, Péter G.; Kecskes, M. L.; Rudolph, K.

doi:10.1046/j.1439-0434.1999.00413.x

Cited by 10 publications

(33 citation statements)

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“…syringae hrcC - prevented development of HR upon a second infiltration (4, 5 or 6 hours later) with the incompatible strain P. syringae pv. syringae 61 , as expected [17]. When PIP was injected into tobacco leaves in combination with P. syringae pv.…”

Section: Resultssupporting

confidence: 80%

“…Later on we found that this local resistance can not only be induced by heat-killed pathogens, but also by saprobic bacteria and some hrp/hrc mutants; i.e. pathogens mutated in their hypersensitivity and pathogenicity genes, many of which code for elements of the Type III Protein Secretion System (T3SS) [17]. Based on our previous findings we regard the local resistance of tobacco as a manifestation of PTI.…”

Section: Introductionmentioning

confidence: 92%

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Pattern Triggered Immunity (PTI) in Tobacco: Isolation of Activated Genes Suggests Role of the Phenylpropanoid Pathway in Inhibition of Bacterial Pathogens

et al. 2014

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BackgroundPattern Triggered Immunity (PTI) or Basal Resistance (BR) is a potent, symptomless form of plant resistance. Upon inoculation of a plant with non-pathogens or pathogenicity-mutant bacteria, the induced PTI will prevent bacterial proliferation. Developed PTI is also able to protect the plant from disease or HR (Hypersensitive Response) after a challenging infection with pathogenic bacteria. Our aim was to reveal those PTI-related genes of tobacco (Nicotiana tabacum) that could possibly play a role in the protection of the plant from disease.Methodology/Principal FindingsLeaves were infiltrated with Pseudomonas syringae pv. syringae hrcC- mutant bacteria to induce PTI, and samples were taken 6 and 48 hours later. Subtraction Suppressive Hybridization (SSH) resulted in 156 PTI-activated genes. A cDNA microarray was generated from the SSH clone library. Analysis of hybridization data showed that in the early (6 hpi) phase of PTI, among others, genes of peroxidases, signalling elements, heat shock proteins and secondary metabolites were upregulated, while at the late phase (48 hpi) the group of proteolysis genes was newly activated. Microarray data were verified by real time RT-PCR analysis. Almost all members of the phenyl-propanoid pathway (PPP) possibly leading to lignin biosynthesis were activated. Specific inhibition of cinnamic-acid-4-hydroxylase (C4H), rate limiting enzyme of the PPP, decreased the strength of PTI - as shown by the HR-inhibition and electrolyte leakage tests. Quantification of cinnamate and p-coumarate by thin-layer chromatography (TLC)-densitometry supported specific changes in the levels of these metabolites upon elicitation of PTI.Conclusions/SignificanceWe believe to provide first report on PTI-related changes in the levels of these PPP metabolites. Results implicated an actual role of the upregulation of the phenylpropanoid pathway in the inhibition of bacterial pathogenic activity during PTI.

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Section: Resultssupporting

confidence: 80%

Section: Introductionmentioning

confidence: 92%

Pattern Triggered Immunity (PTI) in Tobacco: Isolation of Activated Genes Suggests Role of the Phenylpropanoid Pathway in Inhibition of Bacterial Pathogens

et al. 2014

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“…As the effect in PA5Δ fliC , the flagellin of PA5 also impaired the HR induced by HL1, whereas the flagellin of A. tumefaciens (Agro-flg) had no effect (Figure 7A). Based on the previous research [30], infiltration of a non-pathogen results in basal resistance, which is evident by the failure of a challenge inoculation six hours later to elicit the HR in the tobacco and moreover, the PAMP elicitor flg22 was also able to defeat the challenge of HR elicitation by Pto DC3000 in N . benthamiana [11].…”

Section: Resultsmentioning

confidence: 97%

Plant Innate Immunity Induced by Flagellin Suppresses the Hypersensitive Response in Non-Host Plants Elicited by Pseudomonas syringae pv. averrhoi

et al. 2012

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A new pathogen, Pseudomonas syringae pv. averrhoi (Pav), which causes bacterial spot disease on carambola was identified in Taiwan in 1997. Many strains of this pathovar have been isolated from different locations and several varieties of hosts. Some of these strains, such as HL1, are nonmotile and elicit a strong hypersensitive response (HR) in nonhost tobacco leaves, while other strains, such as PA5, are motile and elicit a weak HR. Based on the image from a transmission electron microscope, the results showed that HL1 is flagellum-deficient and PA5 has normal flagella. Here we cloned and analyzed the fliC gene and glycosylation island from Pav HL1 and PA5. The amino acid sequences of FliC from HL1 and PA5 are identical to P. s. pvs. tabaci (Pta), glycinea and phaseolicola and share very high similarity with other pathovars of P. syringae . In contrast to the flagellin mutant PtaΔ fliC , PA5Δ fliC grows as well as wild type in the host plant, but it elicits stronger HR than wild type does in non-host plants. Furthermore, the purified Pav flagellin, but not the divergent flagellin from Agrobacterium tumefaciens , is able to impair the HR induced by PA5Δ fliC . PA5Δ fgt1 possessing nonglycosylated flagella behaved as its wild type in both bacterial growth in host and HR elicitation. Flagellin was infiltrated into tobacco leaves either simultaneously with flagellum-deficient HL1 or prior to the inoculation of wild type HL1, and both treatments impaired the HR induced by HL1. Moreover, the HR elicited by PA5 and PA5Δ fliC was enhanced by the addition of cycloheximide, suggesting that the flagellin is one of the PAMPs (pathogen-associated molecular patterns) contributed to induce the PAMP-triggered immunity (PTI). Taken together, the results shown in this study reveal that flagellin in Pav is capable of suppressing HR via PTI induction during an incompatible interaction.

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“…The defense is defined as basal defense and is reportedly induced by hrp-deficient bacterial pathogens (Klement et al, 1999;Szatmari et al, 2005). Basal defense is also activated by virulent pathogens on susceptible hosts (Jones and Dangl, 2006).…”

Section: Discussionmentioning

confidence: 99%

S-Glycoprotein-Like Protein Regulates Defense Responses in Nicotiana Plants against Ralstonia solanacearum

et al. 2010

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RsRGA4 (for Ralstonia solanacearum-responsive gene A4) encodes a polypeptide similar to S-locus glycoprotein (SGP) from Brassica rapa and SGP-like proteins from Ipomoea trifida and Medicago truncatula. Therefore, we designated RsRGA4 as NtSGLP (for Nicotiana tabacum SGP-like protein) and NbSGLP (its Nicotiana benthamiana ortholog). NbSGLP is expressed in root, leaf, petal, gynoecium, and stamen. Expression of NbSGLP was strongly induced by inoculation with an avirulent strain of R. solanacearum (Rs8107) and slightly enhanced by inoculation with virulent R. solanacearum (RsOE1-1). Expression of NbSGLP was induced by inoculation with an hrpY-deficient mutant of RsOE1-1 and Rs8107. Expression was also induced by aminocyclopropane carboxylic acid and salicylic acid. Virus-induced gene silencing of NbSGLP enhanced the growth of Rs8107. Growth of RsOE1-1 and appearance of wilt symptoms were also accelerated in silenced plants. Expression of PR-1a and EREBP was reduced, and markers for basal defense, such as callose deposition and reduced vascular flow, were compromised in NbSGLP-silenced plants. Moreover, growth of Pseudomonas cichorii, Pseudomonas syringae pv tabaci, and P. syringae pv mellea was also enhanced in the silenced plants. On the other hand, silencing of NbSGLP did not interfere with the appearance of the hypersensitive response. NbSGLP was secreted in a signal peptide-dependent manner. Agrobacterium tumefaciens-mediated expression of NbSGLP induced PR-1a and EREBP expression, callose deposition, and reduced vascular flow. NbSGLP-induced callose deposition and reduced vascular flow were not observed in salicylic acid-deficient N. benthamiana NahG plants. Taken together, SGLP might have a role in the induction of basal defense in Nicotiana plants.

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Symptomless Resistant Response Instead of the Hypersensitive Reaction in Tobacco Leaves after Infiltration of Heterologous Pathovars of Pseudomonas syringae

Cited by 10 publications

References 0 publications

Pattern Triggered Immunity (PTI) in Tobacco: Isolation of Activated Genes Suggests Role of the Phenylpropanoid Pathway in Inhibition of Bacterial Pathogens

Pattern Triggered Immunity (PTI) in Tobacco: Isolation of Activated Genes Suggests Role of the Phenylpropanoid Pathway in Inhibition of Bacterial Pathogens

Plant Innate Immunity Induced by Flagellin Suppresses the Hypersensitive Response in Non-Host Plants Elicited by Pseudomonas syringae pv. averrhoi

S-Glycoprotein-Like Protein Regulates Defense Responses in Nicotiana Plants against Ralstonia solanacearum

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