New diseases of humans, animals and plants emerge regularly. Enhanced virulence on a new host can be facilitated by the acquisition of novel virulence factors. Interspecific gene transfer is known to be a source of such virulence factors in bacterial pathogens (often manifested as pathogenicity islands in the recipient organism) and it has been speculated that interspecific transfer of virulence factors may occur in fungal pathogens. Until now, no direct support has been available for this hypothesis. Here we present evidence that a gene encoding a critical virulence factor was transferred from one species of fungal pathogen to another. This gene transfer probably occurred just before 1941, creating a pathogen population with significantly enhanced virulence and leading to the emergence of a new damaging disease of wheat.

Plant disease resistance is often conferred by genes with nucleotide binding site (NBS) and leucine-rich repeat (LRR) or serine/threonine protein kinase (S/TPK) domains. Much less is known about mechanisms of susceptibility, particularly to necrotrophic fungal pathogens. The pathogens that cause the diseases tan spot and Stagonospora nodorum blotch on wheat produce effectors (host-selective toxins) that induce susceptibility in wheat lines harboring corresponding toxin sensitivity genes. The effector ToxA is produced by both pathogens, and sensitivity to ToxA is governed by the Tsn1 gene on wheat chromosome arm 5BL. Here, we report the cloning of Tsn1 , which was found to have disease resistance gene-like features, including S/TPK and NBS-LRR domains. Mutagenesis revealed that all three domains are required for ToxA sensitivity, and hence disease susceptibility. Tsn1 is unique to ToxA-sensitive genotypes, and insensitive genotypes are null. Sequencing and phylogenetic analysis indicated that Tsn1 arose in the B-genome diploid progenitor of polyploid wheat through a gene-fusion event that gave rise to its unique structure. Although Tsn1 is necessary to mediate ToxA recognition, yeast two-hybrid experiments suggested that the Tsn1 protein does not interact directly with ToxA. Tsn1 transcription is tightly regulated by the circadian clock and light, providing further evidence that Tsn1 -ToxA interactions are associated with photosynthesis pathways. This work suggests that these necrotrophic pathogens may thrive by subverting the resistance mechanisms acquired by plants to combat other pathogens.

Inoculation of one true leaf of cucumber (Cucumis sativus L.) plants with Pseudomonas syringae pathovar syringae results in the systemic appearance of salicylic acid in the phloem exudates from petioles above, below, and at the site of inoculation. Analysis of phloem exudates from the petioles of leaves 1 and 2 demonstrated that the earliest increases in salicylic acid occurred 8 hours after inoculation of leaf 1 in leaf 1 and 12 hours after inoculation of leaf 1 in leaf 2. Detaching leaf I at intervals after inoculation demonstrated that leaf I must remain attached for only 4 hours after inoculation to result in the systemic accumulation of salicylic acid. Because the levels of salicylic acid in phloem exudates from leaf I did not increase to detectable levels until at least 8 hours after inoculation with P. s. pathovar syringae, the induction of increased levels of salicylic acid throughout the plant are presumably the result of another chemical signal generated from leaf I within 4 hours after inoculation. Injection of salicylic acid into tissues at concentrations found in the exudates induced resistance to disease and increased peroxidase activity. Our results support a role for salicylic acid as an endogenous inducer of resistance, but our data also suggest that salicylic acid is not the primary systemic signal of induced resistance in cucumber.Inoculation of one leaf of cucumber plants and other cucurbits with necrotic lesion-inducing pathogens (7-9) or necrosis/chlorosis-inducing chemicals (3, 4) results in the expression of systemic resistance against disease caused by a number of pathogens. The onset of resistance has been correlated with the initial appearance of necrotic lesions and generally begins to develop 3 to 4 d after the resistance-inducing inoculation (7-9).We have recently demonstrated that systemic resistance can be induced in cucumber within 24 h by inoculating leaf with the HR2-inducing bacterium Pseudomonas syringae pv syringae (17 demonstrated that this leaf must remain attached for only 6 h to result in the systemic expression of enhanced peroxidase activity and a small, but detectable, increase in the level of systemic disease resistance. Allowing the first leaf to remain on the plant for up to 12 h after inoculation with P. s. pv syringae resulted in a further increase in the level of systemic resistance as compared with plants that had the inoculated first leaf detached 6 h after inoculation. TnS mutants of P. s. pv syringae that had lost the ability to induce the HR were also unable to induce systemic resistance and peroxidase activity.Dean and Kuc (1, 2) have provided strong evidence that the systemic signal(s) for induced resistance was generated in and mobilized out of the leaves that were initially inoculated ("source" leaves) with resistance-inducing pathogens. Metraux et al. ( 12) recently reported that cucumber plants inoculated with either Colletotrichum lagenarium or tobacco necrosis virus on one leaf had higher levels of salicylic acid (an exogenous inducer ofres...

The necrotrophic fungus Stagonospora nodorum produces multiple proteinaceous host-selective toxins (HSTs) which act in effector triggered susceptibility. Here, we report the molecular cloning and functional characterization of the SnTox3-encoding gene, designated SnTox3, as well as the initial characterization of the SnTox3 protein. SnTox3 is a 693 bp intron-free gene with little obvious homology to other known genes. The predicted immature SnTox3 protein is 25.8 kDa in size. A 20 amino acid signal sequence as well as a possible pro sequence are predicted. Six cysteine residues are predicted to form disulfide bonds and are shown to be important for SnTox3 activity. Using heterologous expression in Pichia pastoris and transformation into an avirulent S. nodorum isolate, we show that SnTox3 encodes the SnTox3 protein and that SnTox3 interacts with the wheat susceptibility gene Snn3. In addition, the avirulent S. nodorum isolate transformed with SnTox3 was virulent on host lines expressing the Snn3 gene. SnTox3-disrupted mutants were deficient in the production of SnTox3 and avirulent on the Snn3 differential wheat line BG220. An analysis of genetic diversity revealed that SnTox3 is present in 60.1% of a worldwide collection of 923 isolates and occurs as eleven nucleotide haplotypes resulting in four amino acid haplotypes. The cloning of SnTox3 provides a fundamental tool for the investigation of the S. nodorum–wheat interaction, as well as vital information for the general characterization of necrotroph–plant interactions.

A toxin, designated SnTox1, was partially purified from culture filtrates of isolate Sn2000 of Stagonospora nodorum, the causal agent of wheat leaf and glume blotch. The toxin showed selective action on several different wheat genotypes, indicating that it is a host-selective toxin (HST). The toxic activity was reduced when incubated at 50 degrees C and activity was eliminated when treated with proteinase K, suggesting that the HST is a protein. The synthetic hexaploid wheat W-7984 and hard red spring wheat Opata 85, the parents of the International Triticeae Mapping Initiative (ITMI) mapping population, were found to be sensitive and insensitive, respectively, to SnTox1. The ITMI mapping population was evaluated for toxin reaction and used to map the gene conditioning sensitivity. This gene, designated Snn1, mapped to the distal end of the short arm of chromosome 1B. The wheat cv. Chinese Spring (CS) and all CS nullisomic-tetrasomic lines were sensitive to the toxin, with the exception of N1BT1D. Insensitivity also was observed when the 1B chromosome of CS was substituted with the 1B chromosome of an insensitive accession of Triticum dicoccoides. In addition, a series of 1BS chromosome deletion lines were used to physically localize the sensitivity gene. Physical mapping indicated that Snn1 lies within a major gene-rich region on 1BS. This is the first report identifying a putative proteinaceous HST from S. nodorum and the chromosomal location of a host gene conferring sensitivity.