Pattern 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. Leaves 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. We 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.

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 hours 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 Pseudomonas 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 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.

IPeach (Prunus persica L. Batsch) is an economically important crop in Hungary. Current production is in ca. 6000 ha of commercial orchards. In July 2017 samples from 2 to 14 year old peach trees (P. persica cvs. Royal Summer, Royal Time, Cresthaven, O’Henry and Redkal) showing leaf and fruit spot symptoms were collected in a 100 ha commercial orchard in Pest County, Hungary. Disease incidence on leaves ranged from a low of 80% relative humidity) but not on water-treated controls. The original pathogen was re-isolated from lesions of inoculated leaves and its identity was confirmed by duplex-PCR (Pothier et al. 2011). To our knowledge, this is the first confirmed report on occurrence of X. arboricola pv. pruni on P. persica in Hungary, previously identified only on Prunus salicina by local plant protection service and on P. armeniaca (Schwarczinger et al. 2017). Bacterial spot of stone fruits is one of the most significant diseases of Prunus species included in the EPPO A2 list of pests recommended for regulation for European Union members. Similar symptoms on peach and apricot were recently reported by growers from two neighboring counties, indicating pathogen spread. Therefore Xap could have a significant impact on peach production in Hungary. References: Ballard, E. L., et al. Plant Dis. 95:1109, 2011. Parkinson, N., et al. Int. J. Syst. Evol. Microbiol. 57:2881, 2007. Pothier, J. F., et al. J. Microbiol. Meth. 86:16, 2011. Schaad, N. W. et al. (eds.) Laboratory Guide for Identification of Plant Pathogenic Bacteria, 3rd ed. APS, St. Paul, MN., 2001. Schwarczinger, I., et al. Plant Dis. 101:1031, 2017.

In June 2018 leaf spot symptoms suggesting Xanthomonas arboricola pv. pruni (Xap) infection were detected on almond (Prunus dulcis) cv. ‘Fournat de Brezenaud’ and later, in October also on almond c...