Colonization of the leaf vasculature by Xanthomonas campestris pv. campestris

Xanthomonas campestris pv. campestris (Xcc) is the causal agent of Black rot disease in Brassica crops. This bacterium invades the vasculature via hydathodes, tiny organs scattered along the leaf margin. How plants defend this entry point against pathogens is poorly understood. This PhD thesis reports that two key plant immune hubs, BAK1 and EDS1, restrict bacterial colonization inside hydathodes in the model plant Arabidopsis. Notably, hydathode immunity proved to be effective against both adapted (Xcc) and non-hydathode adapted bacteria. To improve hydathode immunity studies, a new method to quantify bacterial disease and spread was then developed. The focus then shifts to the bacterium. How does Xcc gain access to the vasculature upon hydathode colonization? A pangenome comparison of Xcc and its non-vascular relative X. campestris pv. raphani (Xcr) revealed that Xcc emerged from Xcr, and that this event coincided with increased acquisition of mobile genetic elements, plasmids, and virulence factors, and the loss of CRISPR-Cas in Xcc. Presumably, loss of the CRISPR-Cas locus lowered the bacterial genomic defense. Interestingly, in Xcc the CRISPR-Cas locus is replaced by a gene coding for a virulence factor (XopN). Finally, the pangenome analysis revealed four cell wall degrading enzymes specific for Xcc. These enzymes, as well as the type II secretion system, were shown to be required for vascular colonization. Together, this PhD thesis unveils novel mechanisms in the battle between plants and bacteria over access to the leaf vasculature through hydathodes.