Many plant-associated microbes are pathogens that impair plant growth and reproduction. Plants respond to infection using a two-branched innate immune system. The first branch recognizes and responds to molecules common to many classes of microbes, including non-pathogens. The second responds to pathogen virulence factors, either directly or through their effects on host targets. These plant immune systems, and the pathogen molecules to which they respond, provide extraordinary insights into molecular recognition, cell biology and evolution across biological kingdoms. A detailed understanding of plant immune function will underpin crop improvement for food, fibre and biofuels production.

http://www.segenetica.es/cng2/cng2008/biblio/Ref-Marc-Valls---Jones-and-Dangl-Nat06.pdf

The plant immune system

Plants cannot move to escape environmental challenges. Biotic stresses result from a battery of potential pathogens: fungi, bacteria, nematodes and insects intercept the photosynthate produced by plants, and viruses use replication machinery at the host's expense. Plants, in turn, have evolved sophisticated mechanisms to perceive such attacks, and to translate that perception into an adaptive response. Here, we review the current knowledge of recognition-dependent disease resistance in plants. We include a few crucial concepts to compare and contrast plant innate immunity with that more commonly associated with animals. There are appreciable differences, but also surprising parallels.

Plant pathogens and integrated defence responses to infection.

It has been suggested that effective defense against biotrophic pathogens is largely due to programmed cell death in the host, and to associated activation of defense responses regulated by the salicylic acid-dependent pathway. In contrast, necrotrophic pathogens benefit from host cell death, so they are not limited by cell death and salicylic acid-dependent defenses, but rather by a different set of defense responses activated by jasmonic acid and ethylene signaling. This review summarizes results from Arabidopsis-pathogen systems regarding the contributions of various defense responses to resistance to several biotrophic and necrotrophic pathogens. While the model above seems generally correct, there are exceptions and additional complexities.

Contrasting Mechanisms of Defense Against Biotrophic and Necrotrophic Pathogens

Gram-negative bacteria characteristically are surrounded by an additional membrane layer, the outer membrane. Although outer membrane components often play important roles in the interaction of symbiotic or pathogenic bacteria with their host organisms, the major role of this membrane must usually be to serve as a permeability barrier to prevent the entry of noxious compounds and at the same time to allow the influx of nutrient molecules. This review summarizes the development in the field since our previous review (H. Nikaido and M. Vaara, Microbiol. Rev. 49:1-32, 1985) was published. With the discovery of protein channels, structural knowledge enables us to understand in molecular detail how porins, specific channels, TonB-linked receptors, and other proteins function. We are now beginning to see how the export of large proteins occurs across the outer membrane. With our knowledge of the lipopolysaccharide-phospholipid asymmetric bilayer of the outer membrane, we are finally beginning to understand how this bilayer can retard the entry of lipophilic compounds, owing to our increasing knowledge about the chemistry of lipopolysaccharide from diverse organisms and the way in which lipopolysaccharide structure is modified by environmental conditions.

Molecular Basis of Bacterial Outer Membrane Permeability Revisited

Rapid generation of superoxide and accumulation of H2O2 is a characteristic early feature of the hypersensitive response following perception of pathogen avirulence signals. Emerging data indicate that the oxidative burst reflects activation of a membrane-bound NADPH oxidase closely resembling that operating in activated neutrophils. The oxidants are not only direct protective agents, but H2O2 also functions as a substrate for oxidative cross-linking in the cell wall, as a threshold trigger for hypersensitive cell death, and as a diffusible signal for induction of cellular protectant genes in surrounding cells. Activation of the oxidative burst is a central component of a highly amplified and integrated signal system, also involving salicylic acid and perturbations of cytosolic Ca2+, which underlies the expression of disease-resistance mechanisms.

The oxidative burst in plant disease resistance

Type III secretion systes are highly conserved among gram-negative plant and animal pathogenic bacteria. Through the type III secretion system, bacteria inject a number of virulence proteins into the host cells. Analysis of the whole genome sequence of Pseudomonas syringae pv. tomato DC3000 strain identified a locus, named HopPtoF, that is homologous to the avirulence gene locus avrPphF in P. syringae pv. phaseolicola. The HopPtoF locus harbors two genes, ShcFPto and HopFPto, that are preceded by a single hrp box promoter. We present evidence here to show that ShcFPto and HopFPto encode a type III chaperone and a cognate effector, respectively. ShcFPto interacts with and stabilizes the HopFPto protein in the bacterial cell. Translation of HopFPto starts at a rare initiation codon ATA that limits the synthesis of the HopFPto protein to a low level in bacterial cells.

/pdf/the-hopptof-locus-of-pseudomonas-syringae-pv-tomato-dc3000-25f2f5zrgl.pdf

The HopPtoF locus of Pseudomonas syringae pv. tomato DC3000 encodes a type III chaperone and a cognate effector.

Since the early 1990's, bacterial blight has emerged as an important disease of cantaloupe in France, particularly in the south-west but has caused epidemics in all the production regions of this country. The pathogen is a complex composed of strains identified as Pseudomonas syringae pv. aptata (70% of the strains) and the remaining resembling P. viridijlava (2%), P. s. pv. lachrymans (1%) or P. syringae in general but with no correspondence to a known pathovar. To investigate the epidemiology of this disease and to develop disease control strategies, we have attempted to identify sources of inoculum in the field, factors contributing to the explosive development of the disease, resistance of the bacterium to copper pesticides, and sources of disease resistance in Cucumis melo. Based on our observations and on the description of possible outbreaks of this disease elsewhere in the world, we report here a hypothetical scenario of the critical factors triggering disease development and of the potential efficiency of different control strategies.

Pseudomonas syringae and related pathogens

Virtually all crop plants are attacked by pathogenic microbes, including bacteria, fungi, oomycetes, and nematodes. In many cases, bacterial diseases are still poorly controlled with century-old agents like copper, and cause serious losses, as seen with the recent citrus canker outbreak in Florida

/pdf/lifestyles-of-the-effector-rich-genome-enabled-1szbd6t5lz.pdf

Lifestyles of the effector rich: genome-enabled characterization of bacterial plant pathogens.

Pseudomonas syringae pv. tomato DC3000 and its derivatives cause disease in tomato, Arabidopsis and Nicotiana benthamiana. The primary virulence factors include a repertoire of 29 effector proteins injected into plant cells by the type III secretion system and the phytotoxin coronatine. The complete repertoire of effector genes and key coronatine biosynthesis genes have been progressively deleted and minimally reassembled to reconstitute basic pathogenic ability in N. benthamiana, and in Arabidopsis plants that have mutations in target genes that mimic effector actions. This approach and molecular studies of effector activities and plant immune system targets have highlighted a small subset of effectors that contribute to essential processes in pathogenesis. Most notably, HopM1 and AvrE1 redundantly promote an aqueous apoplastic environment, and AvrPtoB and AvrPto redundantly block early immune responses, two conditions that are sufficient for substantial bacterial growth in planta. In addition, disarmed DC3000 polymutants have been used to identify the individual effectors responsible for specific activities of the complete repertoire and to more effectively study effector domains, effector interplay and effector actions on host targets. Such work has revealed that AvrPtoB suppresses cell death elicitation in N. benthamiana that is triggered by another effector in the DC3000 repertoire, highlighting an important aspect of effector interplay in native repertoires. Disarmed DC3000 polymutants support the natural delivery of test effectors and infection readouts that more accurately reveal effector functions in key pathogenesis processes, and enable the identification of effectors with similar activities from a broad range of other pathogens that also defeat plants with cytoplasmic effectors.

Defining essential processes in plant pathogenesis with Pseudomonas syringae pv. tomato DC3000 disarmed polymutants and a subset of key type III effectors.

The hrpC operon of Erwinia chrysanthemi EC16 encodes five genes conserved in Erwinia amylovora and Pseudomonas syringae. Mutagenesis indicated that hrcC is required for elicitation of the hypersensitive reaction in tobacco leaves. The unexpected presence of plcA and homologs of hemolysin/activator genes in the regions flanking the hrcC and hrpN operons is reported.

The hrpC and hrpN operons of Erwinia chrysanthemi EC16 are flanked by plcA and homologs of hemolysin/adhesin genes and accompanying activator/transporter genes.

Alan Collmer

Papers

The HopPtoF locus of Pseudomonas syringae pv. tomato DC3000 encodes a type III chaperone and a cognate effector.

Pseudomonas syringae and related pathogens

Lifestyles of the effector rich: genome-enabled characterization of bacterial plant pathogens.

Defining essential processes in plant pathogenesis with Pseudomonas syringae pv. tomato DC3000 disarmed polymutants and a subset of key type III effectors.

The hrpC and hrpN operons of Erwinia chrysanthemi EC16 are flanked by plcA and homologs of hemolysin/adhesin genes and accompanying activator/transporter genes.