Type IV pili also function in bacterial conjugation (Proft & Baker, 2009), an active mechanism within biofilm cells, being responsible for the transference

of genetic material including genes of resistance against antibiotics (Molin & Tolker-Nielsen, 2003). Interestingly, the treatment of X. fastidiosa with gomesin upregulated the expression of plasmid genes, including one gene encoding a conjugal transfer protein (traG or virB11). Besides involvement in adhesion to substrata and cell-to-cell aggregation, see more bacterial biofilms are also involved in bacterial resistance to many antimicrobial agents (Mah & O’Toole, 2001). In addition to the upregulation of CDS related to biofilms, the treatment of X. fastidiosa with a sublethal concentration of gomesin indeed leads to an enhancement in biofilm production. This does not seem to be a general effect to all antimicrobial agents, because exposure of X. fastidiosa to a sublethal concentration of streptomycin showed no effects on biofilm production. It has been reported that bacteria treated with sublethal concentrations of antimicrobial agents can increase or diminish biofilm production (Drenkard & Ausubel, 2002; Overhage et al., 2008; Jones et al., 2009). In Neisseria meningitidis, a sublethal concentration of

LL-37, a human cathelicidin, induces the formation of the a polysaccharide capsule (Jones et al., 2009). Conversely, this same AMP was reported to inhibit the biofilm production by Pseudomonas aeruginosa (Overhage et al., 2008). On the other hand, conventional selleck chemical antibiotics were reported to stimulate biofilm production by this same bacterium (Drenkard & Ausubel, 2002). These

results clearly demonstrate that the response of bacteria to a sublethal concentration of antimicrobial agents depends not only on the bacterial strain but also on the nature of the drug. When X. fastidiosa pre-exposed to 50 μM of gomesin was inoculated into tobacco plants, nearly fewer plants displayed foliar lesions relative to control plants (inoculated with nontreated bacteria) 30 days after inoculation (Fig. 3). This result suggests that due to the enhancement in biofilm production, bacteria may be trapped to fewer vessels of the plant xylem, causing a delay in the appearance of symptoms. Indeed, the above-described mutants of the X. fastidiosa Temecula strain defective for the production of the hemagglutinin HxfA, despite having a reduced ability to adhere to a glass surface and also to form cell-to-cell aggregates, were surprisingly hypervirulent to grapevine, due to an increased number of infected vessels of the plant xylem (Guilhabert & Kirkpatrick, 2005). On the other hand, limiting bacteria to a few vessels of the plant could have the opposite effect, diminishing disease symptoms. Together, our results demonstrate that gomesin modulates the global gene expression of X. fastidiosa at a sublethal concentration, inducing genes involved in biofilm production, among others. Indeed, X.