We also observed that LPA-induced VEGF-C was abolished by NAC

lts indicate that BAK1, BIK1 and MAP3K, and NPR1, EIN2, COl1 and PR4 genes are activated in response to SSBXoc or Hpa1. The data show that SSBXoc triggers a cascade of events similar to those triggered by Flg22, which leads to the oxidative burst and callose deposition and activates the expression of PR genes. These results support our presumption that SSBXoc acts as a PAMP like Hpa1. SSBXoc-elicited HR is a form of Programmed Cell Death The next experiments were designed to determine whether SSBXoc, like Hpa1, is toxic to plant cells or not and SSBXoc leads to a metabolic response that triggers HR. Three 21147071 metabolic inhibitors were used: actinomycin D, cycloheximide, and LaCl3. These inhibitors were incubated with purified SSBXoc and then assayed for HR induction in tobacco. All three inhibitors prevented the SSBXoc-elicited HR in (-)-Blebbistatin web tobacco when co-infiltrated with the purified SSBXoc. These results indicated that the SSBXoc-elicited HR is an active process and requires de novo gene expression, protein synthesis and calcium flux across membranes. Thus, SSBXoc acts as an elicitor, like Hpa1, of HR but is not directly toxic to plant cells. It is well-documented that harpin-elicited HR is a form of programmed cell death, which is accompanied by DNA laddering. To determine whether the SSBXoc-elicited HR is a form of PCD, DNA laddering experiments were performed. Total genomic DNA from SSBXoc-infiltrated tobacco leaves were extracted at different time points after infiltration and analyzed on 2% agarose gels. As shown in Fig. 2E, DNA ladders were clearly observed in SSBXoc-inoculated leaves at 24 hpi, 12 h later than that in Hpa1-inoculated leaves. Thus, SSBXoc, like Hpa1, elicits PCD that is characterized by DNA laddering. We then investigated whether SSBXoc-elicited HR occurs with the activation of known HR marker genes including HIN1 , HSR203J, and the SA-dependent marker, PR1a; the JA-dependent gene, PR1b, was also conducted. The expression of these genes was evaluated in tobacco leaves infiltrated with SSBXoc, Hpa1, and EVP 6 hpi. All four genes were induced in response to SSBXoc; however, Hpa1 did not induce the SSBXoc Induces Plant Disease Resistance and Promotes Plant Growth Tobacco infiltrated with SSBXoc shows elevated expression of SA- and JA-dependent genes, along with the oxidative burst and callose deposition. Therefore, we hypothesized that SSBXoc may stimulate induced resistance to pathogen infection. For this, we inoculated a fungal pathogen, A. alternata TBA28A, causal agent of tobacco brown spot disease, to fully-expanded tobacco leaves that were previously sprayinoculated twice with SSBXoc in three-day intervals. The necrotic areas in tobacco leaves treated with SSBXoc were significantly smaller than those observed on leaves inoculated with EVP. Like SSBXoc, we found that Hpa1 also induced similar resistance to A. alternata. The data suggest that both SSBX 11358331 and Hpa1 induce SAR against pathogen infection. Xanthomonas SSB Protein Acts as Harpins 7 Xanthomonas SSB Protein Acts as Harpins The application of a harpin, HrpN from E. amylovora, enhances plant growth, particularly because the Eth-dependent genes are activated. The activation of Eth-dependent genes, e.g. EIN2 and PR4, led us to determine whether SSBXoc promotes plant growth or not. For this, germinating seeds of Arabidopsis thaliana Col-0 and tobacco cv. Xanthi were soaked in a solution containing 1 mM SSBXoc for 8 h and then transferred to MS medium for 14 days. The r