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

Klement, Z.; Bozsó, Zoltán; Ott, Péter G.; Kecskés, Mihály; Rudolph, K.

doi:10.1111/j.1439-0434.1999.tb03852.x

Cited by 26 publications

(25 citation statements)

References 19 publications

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“…According to an earlier hypothesis (Goodman and Novacky 1994;Agrios 1997), incompatible pathogens must induce the HR phenotype in a nonhost plant. However, more recent data have shown that even pathogenic bacteria, which cause severe symptoms on a host plant, will not induce HR on a nonhost plant (Fink et al 1990;Jakobek and Lindgren 1993;Kamoun et al 1998;Klement et al 1999). These results indicated a requirement for a new model to explain Type I nonhost resistance.…”

Section: Resultsmentioning

confidence: 88%

Insight into Types I and II nonhost resistance using expression patterns of defense-related genes in tobacco

Lee

Chung

et al. 2006

Planta

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Plants protect themselves against pathogens using a range of response mechanisms. There are two categories of nonhost resistance: Type I, which does not result in visible cell death; and Type II, which entails localized programmed cell death (or hypersensitive response) in response to nonhost pathogens. The genes responsible for these two systems have not yet been intensively investigated at the molecular level. Using tobacco plants (Nicotiana tabacum), we compared expression of 12 defense-related genes between a Type I (Xanthomonas axonopodis pv. glycines 8ra) nonhost interaction, and two Type II (Pseudomonas syringae pv. syringae 61 and P. syringae pv. phaseolicola NPS3121) nonhost interactions, as well as those expressed during R gene-mediated resistance to Tobacco mosaic virus. In general, expression of most defense-related genes during R gene-mediated resistance was activated 48 h after challenge by TMV; the same genes were upregulated as early as 9 h after infiltration by nonhost pathogens. Surprisingly, X. axonopodis pv. glycines (Type I) elicited the same set of defense-related genes as did two pathovars of P. syringae, despite the absence of visible cell death. In two examples of Type II nonhost interactions, P. syringae pv. phaseolicola NPS3121 produced an expression profile more closely resembling that of X. axonopodis pv. glycines 8ra, than that of P. syringae pv. syringae 61. These results suggest that Type I nonhost resistance may act as a mechanism providing a more specific and active defense response against a broad range of potential pathogens.

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Section: Resultsmentioning

confidence: 88%

Insight into Types I and II nonhost resistance using expression patterns of defense-related genes in tobacco

Lee

Chung

et al. 2006

Planta

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“…Leaf materials were collected at 6 h after inoculations (6 hpi). This sampling time was chosen on the basis of our previous work since PTI develops in tobacco by this time at 20°C as detected by using various marker reactions (Burgyán and Klement, 1979 ; Ott et al, 1997 , 2006 ; Bozsó et al, 1999 , 2005 ; Klement et al, 1999 , 2003 ; Szatmári et al, 2006 , 2014 ).…”

Section: Resultsmentioning

confidence: 99%

Overlapping Yet Response-Specific Transcriptome Alterations Characterize the Nature of Tobacco–Pseudomonas syringae Interactions

et al. 2016

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In this study transcriptomic alterations of bacterially induced pattern triggered immunity (PTI) were compared with other types of tobacco–Pseudomonas interactions. In addition, using pharmacological agents we blocked some signal transduction pathways (Ca2+ influx, kinases, phospholipases, proteasomic protein degradation) to find out how they contribute to gene expression during PTI. PTI is the first defense response of plant cells to microbes, elicited by their widely conserved molecular patterns. Tobacco is an important model of Solanaceae to study resistance responses, including defense mechanisms against bacteria. In spite of these facts the transcription regulation of tobacco genes during different types of plant bacterial interactions is not well-described. In this paper we compared the tobacco transcriptomic alterations in microarray experiments induced by (i) PTI inducer Pseudomonas syringae pv. syringae type III secretion mutant (hrcC) at earlier (6 h post inoculation) and later (48 hpi) stages of defense, (ii) wild type P. syringae (6 hpi) that causes effector triggered immunity (ETI) and cell death (HR), and (iii) disease-causing P. syringae pv. tabaci (6 hpi). Among the different treatments the highest overlap was between the PTI and ETI at 6 hpi, however, there were groups of genes with specifically altered activity for either type of defenses. Instead of quantitative effects of the virulent P. tabaci on PTI-related genes it influenced transcription qualitatively and blocked the expression changes of a special set of genes including ones involved in signal transduction and transcription regulation. P. tabaci specifically activated or repressed other groups of genes seemingly not related to either PTI or ETI. Kinase and phospholipase A inhibitors had highest impacts on the PTI response and effects of these signal inhibitors on transcription greatly overlapped. Remarkable interactions of phospholipase C-related pathways with the proteasomal system were also observable. Genes specifically affected by virulent P. tabaci belonged to various previously identified signaling routes, suggesting that compatible pathogens may modulate diverse signaling pathways of PTI to overcome plant defense.

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“…The reason for using flagellin suspension for inducing BR instead of using the bacteria suspension itself was to avoid false positive protein spots of bacterial proteins on 2D-PAGE gels. Being symptomless, BR had to be detected by an indirect method: inhibition of hypersensitive response (HR; Klement et al 1999). Water-injected as control and flagellin-injected tobacco plants were incubated at 30 °C because BR develops quickly at this temperature.…”

Section: Methodsmentioning

confidence: 99%

Changes in apoplast protein pattern suggest an early role of cell wall structure remodelling in flagellin-triggered basal immunity

Szabó¹,

Szatmári²,

Hunyadi‐Gulyás³

et al. 2012

Biol. plant.

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The leaf apoplast is a dynamic compartment in contact with plant pathogenic bacteria after infection. Among the very first interaction events is the receptor-mediated perception of bacterial surface molecules such as flagellin or other conserved microbe-associated molecular patterns (MAMPs). Apoplast proteins likely play a role in basal resistance (BR) or pattern-triggered immunity (PTI). Here, a proteomic approach was carried out on water soluble -potentially the most mobile -apoplast proteins from flagellin-treated tobacco (Nicotiana tabacum) leaves. As the quickness of BR/PTI seems crucial for its efficacy, samples were taken as early as 2.5 and 7 h post inoculation. Proteins were separated by two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) and identified by liquid chromatography tandem mass spectrometry (LC-MS/MS). Forty-nine different proteins from 28 protein spots changed in their density compared to the water-inoculated control. Eleven protein spots appeared de novo in response to EBR induction. There are glycohydrolases and redox-active proteins besides pathogenesis-related proteins among them, predicting plant cell wall structural modifications and more direct antimicrobial effectors as earliest changes related to BR/PTI.

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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 26 publications

References 19 publications

Insight into Types I and II nonhost resistance using expression patterns of defense-related genes in tobacco

Insight into Types I and II nonhost resistance using expression patterns of defense-related genes in tobacco

Overlapping Yet Response-Specific Transcriptome Alterations Characterize the Nature of Tobacco–Pseudomonas syringae Interactions

Changes in apoplast protein pattern suggest an early role of cell wall structure remodelling in flagellin-triggered basal immunity

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