1). Interestingly, CDS-encoding enzymes involved in exopolysaccharide synthesis (XF2364, XF2366, XF2367 and XF2369), plasmid related (XFa0015 and XFa0027) and surface structures (XF2196, XF0369 and XF0371), which are characteristically related to bacterial biofilms, were found to be upregulated (Table 2). In addition, the expression of genes belonging to functional categories usually activated under stressful conditions, such as toxin

production and detoxification (XF1137, XF1216, XF1341, XF1898 and XF2416), phage related (XF0508, XF 0733, XF1675, XF1718, XF2482, XF2487 and XF2492) and transposons (XF0536), was also induced by gomesin treatment. The biofilm produced by X. fastidiosa upon exposure to 50 μM of gomesin was evaluated and compared with the biofilm produced by nontreated cells. Quizartinib nmr As shown in Fig. 2, we detected a fivefold increase in biofilm production upon gomesin treatment. In contrast, no effect on biofilm formation was observed when X. fastidiosa was exposed to 1 μg mL−1 of streptomycin (Fig. 2), a concentration defined to be sublethal against this bacterium (Table 1). To evaluate whether the treatment with gomesin could interfere with X. fastidiosa virulence, experimental infections of tobacco plants were carried out using bacteria

pre-exposed to either 25 or 50 μM of this AMP. Thirty days after inoculation, plants were inspected for lesions on the axial surface of the leaves, a typical symptom of X. fastidiosa infection in tobacco plant (Lopes et al., 2000). The number of symptomatic plants in the group inoculated with the virulent strain 9a5c of X. fastidiosa pretreated Selleckchem FG4592 with 50 μM of gomesin (22 of 36 plants) was significantly lower than the number of plants of the Cediranib (AZD2171) control group (34 of 36 plants), which was inoculated with nontreated bacteria (Fig. 3). On the other hand, the number of symptomatic

plants among the group challenged with bacteria pretreated with 25 μM of gomesin (31 of 36 plants) was also lower, but not statistically different from the control group (Fig. 3). The reduction in the number of plants exhibiting leaf lesions in the group inoculated with the virulent strain 9a5c exposed to 50 μM of gomesin is not related to a reduction in the bacterial viability, as verified by bacterial growth on 2% PW plates (data not shown). Moreover, no symptomatic plant was detected in the groups inoculated with either gomesin 50 μM or PBS (data not shown), showing that the lesions on the leaves are neither a consequence of a toxic action of gomesin to the plants nor caused by the inoculation process itself. Remarkably, all the plants inoculated with X. fastidiosa, subjected or not to a pretreatment with gomesin, died after approximately 210 additional days. Together, our results show that the pre-exposure of X. fastidiosa to 50 μM of gomesin causes a delay in the onset of foliar lesions on tobacco plants, which may reflect a reduction in bacterial colonization. It has been demonstrated that, in citrus plants, X.