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Elemental sulphur (32S0 detected as 32S8) is the only inorganic phytoalexin recorded, first identified as a component of resistance of Theobroma cacao to Verticillium dahliae. Here we report S0 production in another four, diverse families in response to fungal and bacterial pathogens. S0 was detected in xylem excised from infected but not control tomato and cotton to V. dahliae, tobacco and French bean to Fusarium oxysporum and tomato to Ralstonia solanacearum. Accumulation was more rapid and greater in disease resistant genotypes than in susceptible lines. No S0 was detected in strawberry challenged with V. dahliae or maize leaves with Erwinia stewartii. Furthermore, S0 was absent from leaves of six spp. undergoing hypersensitive reactions to Pseudomonas syringae pathovars. These data suggest that S0 production may be specific to xylem and does not occur in all plants. Anomalously, high constitutive levels of S0 occurred in control and hypersensitively responding leaves of Brassica oleracea, irrespective of challenge by an incompatible race of Peronospora parasitica and in uninoculated Arabidopsis thaliana leaves. Scanning electron microscopy–energy dispersive X-ray microanalysis showed sulphur in A. thaliana was present in all leaf cell types. S8 showed high toxicity (ED50 0.78–3.125 μg ml−1 to spore germination and germ tube growth) to isolates of V. dahliae and F. oxysporum but had no effect on bacterial pathogens or to a Phytophthora sp. Levels in tomato (10 μg g−1) and Arabidopsis (1.5–6 μg g−1) were potentially inhibitory, but in other spp. (maximum 100–250 ng g−1) were below theoretical inhibitory levels. The highly localised accumulation of other phytoalexins and of S0 in T. cacao and tomato xylem, suggest S0 is produced in sufficient amounts, at the right time and place in some interactions to contribute to resistance. [Copyright &y& Elsevier]

Abstract: Extracellular polysaccharide-defective (EPS−) mutants of the cassava blight pathogen, Xanthomonas axonopodis pv. manihotis, were created by targeted disruption of the biosynthetic gene gumD. Pathogenicity of mutants was severely attenuated. Two EPS− mutants infiltrated into the leaf apoplast, caused initial water-soaking and chlorosis but symptoms were confined to inoculated zones, whereas those of wild type I56 rapidly extended and developed into flaccidity. This pattern reflected failure of EPS− mutants to spread. In entire lobes the wild-type population exceeded by 200-fold that of EPS− mutants. Petioles injected with EPS− mutants remained symptomless, in contrast to severe wilting with I56. EPS conferred significant resistance to H2O2, known to be produced by cassava cells during the oxidative burst. At 1h exposure to 1mM peroxide, only 3% EPS− compared with 48% wild type cells survived. Also, EPS− mutants were more vulnerable to UV irradiation. These phenomena correlated with reduced epiphytic survival of EPS− following spray application. The requirement for EPS in pathogenicity and epiphytic fitness is considered. [Copyright &y& Elsevier]

The wheat fungal pathogen Stagonospora nodorum produces an extracellular trypsin-like protease, SNP1, during early stages of hyphal growth on the surface of host leaves and during penetration. Variation of SNP1 mRNA levels and enzyme activity during infection, were correlated with levels of aggressiveness of three wild-type isolates. SNP1 was deleted in two wild-type isolates using a gene replacement strategy. SNP1-deleted mutants completely lacked trypsin activity in vitro and on inoculated wheat leaves, but were not reduced in pathogenicity. SNP1-deleted mutants still have 50% of the total alkaline protease activity of wild-type. This residual activity comes from a previously undetected alkaline protease with subtilisin-like substrate and inhibitor specificities, which is produced in vitro and on host leaves. We hypothesize that this subtilisin protease may act in concert with SNP1 and may compensate for the loss of trypsin protease activity in the SNP1-deletion mutants. [Copyright &y& Elsevier]