Xylella fastidiosa is the etiologic agent of a wide range of plant diseases including citrus variegated chlorosis (CVC), a major threat to the Brazilian citrus industry. The genomes of several strains of this phytopathogen have been completely sequenced, enabling large-scale functional studies. A DNA microarray representing 2608 (91,6%) coding sequences (CDS) of X. fastidiosa CVC strain 9a5c was used to identify genes that were transcriptionally regulated by growth under limiting and excess concentrations of iron. When treated with the iron chelator 2,2-dipyridyl,, 193 CDS were considered as up-regulated and 216 were considered as down-regulated. In the presence of 100uM of ferric pyrophosphate, 218 and 256 CDS were considered as up- and down-regulated, respectively. Differential expression for a subset of 43 CDS was further evaluated by RT-qPCR and the microarray results for 34 of these were confirmed. In order to identify CDS regulated by the ferric uptake regulator (Fur), we have also screened the promoter regions of strain 9a5c genome for putative Fur-boxes. Despite the fact Fur-box like sequences are not ubiquitous in the genome of Xylella, some candidates could be identified. Among these, the promoter region of XF0599, which encodes a receptor for siderophores, displays a Fur-box similar to the Escherichia coli consensus. Recombinant Xf-Fur was used on electrophoretic mobility shift assays (EMSA) for in vitro validation of this putative X. fastidiosa Fur-box (see poster by Lupo, F.N.G. et al. for details). The CDS differentially expressed upon the iron concentration shift participate in diverse cellular functions. Many CDS involved with regulatory functions, pathogenicity and cell structure, were modulated in both conditions tested suggesting that major changes in cell architecture and metabolism occur when X. fastidiosa cells are exposed to extreme variations in iron concentration. Interestingly, the modulated CDS include that related to colicin V synthesis and secretion and to pilli/fimbria functions. Taken together, our data support the hypothesis that Fur is not solely responsible for the modulation of the iron regulon of X. fastidiosa and present novel evidence for iron regulation of pathogenicity determinants.