There is remarkable conservation in the recognition of pathogen-associated molecular patterns (PAMPs) by innate immune responses of plants, insects and mammals. We developed an Arabidopsis thaliana leaf cell system based on the induction of early-defence gene transcription by flagellin, a highly conserved component of bacterial flagella that functions as a PAMP in plants and mammals. Here we identify a complete plant MAP kinase cascade (MEKK1, MKK4/MKK5 and MPK3/MPK6) and WRKY22/WRKY29 transcription factors that function downstream of the flagellin receptor FLS2, a leucine-rich-repeat (LRR) receptor kinase. Activation of this MAPK cascade confers resistance to both bacterial and fungal pathogens, suggesting that signalling events initiated by diverse pathogens converge into a conserved MAPK cascade.

We cloned the rpoN (ntrA, glnF) gene encoding the alternate sigma factor 54 from the opportunistic multihost pathogen Pseudomonas aeruginosa strain PA14. A marker exchange protocol was used to construct the PA14 rpoN insertional mutation rpoN::Gen r . PA14 rpoN::Gen r synthesized reduced levels of pyocyanin and displayed a variety of phenotypes typical of rpoN mutants, including a lack of motility and the failure to grow on nitrate, glutamate, or histidine as the sole nitrogen source. Compared to wild-type PA14, rpoN::Gen r was ca. 100-fold less virulent in a mouse thermal injury model and was significantly impaired in its ability to kill the nematode Caenorhabditis elegans. In an Arabidopsis thaliana leaf infectivity assay, although rpoN::Gen r exhibited significantly reduced attachment to trichomes, stomata, and the epidermal cell surface, did not attach perpendicularly to or perforate mesophyll cell walls, and proliferated less rapidly in Arabidopsis leaves, it nevertheless elicited similar disease symptoms to wild-type P. aeruginosa PA14 at later stages of infection. rpoN::Gen r was not impaired in virulence in a Galleria mellonella (greater wax moth) pathogenicity model. These data indicate that rpoN does not regulate the expression of any genes that encode virulence factors universally required for P. aeruginosa pathogenicity in diverse hosts.In gram-negative bacteria, the alternate sigma factor 54 , working in concert with a transcriptional activator that belongs to the NtrC superfamily, activates a variety of genes that are regulated in response to external stimuli (1). For example, in various bacteria, 54 is required for expression of the enzymatic pathways responsible for nitrogen utilization, dicarboxylate transport, xylene degradation, and hydrogen utilization (6,32,39,41,61). 54 is also involved in the regulation of virulence-related factors in both plant and animal pathogens, including pilin, flagellin, and alginate synthesis in Pseudomonas aeruginosa (19,58,60); capsular expression in Klebsiella pneumoniae (3); and regulation of hrp gene expression and coronatine biosynthesis in Pseudomonas syringae (23,24).Our laboratory has developed a bacterial pathogenicity model that utilizes a clinical isolate of P. aeruginosa (strain UCBPP-PA14 [referred to here as PA14]) that elicits severe soft-rot-like symptoms and proliferates when infiltrated into Arabidopsis leaves (52), kills the larvae of the wax moth caterpillar Galleria mellonella (30), causes lethal sepsis in a mouse full-skin-thickness burn model (52), and kills the nematode Caenorhabditis elegans (40,56,57). Interestingly, there is significant overlap among the PA14 virulence factors required for pathogenesis in plants, nematodes, insects, and mice. For example, among 21 genes identified as being involved in pathogenesis by screening transposon-induced PA14 mutants in plants and nematodes, 18, 17, 19, and 21 of these genes were required for pathogenicity in Arabidopsis, nematodes, wax moths, and mice, respectively (30,40,53,57).In other studies...

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