Botrytis cinerea is responsible for the gray mold disease on more than 200 host plants. This necrotrophic ascomycete displays the capacity to kill host cells through the production of toxins, reactive oxygen species and the induction of a plant-produced oxidative burst. Thanks to an arsenal of degrading enzymes, B. cinerea is then able to feed on different plant tissues. Recent molecular approaches, for example on characterizing components of signal transduction pathways, show that this fungus shares conserved virulence factors with other phytopathogens, but also highlight some Botrytis-specific features. The discovery of some first strain-specific virulence factors, together with population data, even suggests a possible host adaptation of the strains. The availability of the genome sequence now stimulates the development of high-throughput functional analysis to decipher the mechanisms involved in the large host range of this species.

Gametophytic self-incompatibility in the Solanaceae is controlled by a single, nultiafleic locus, the S locus.We have recently described an allele of the S locus of Lycopersicon peruvianum that caused this normally self-incompatible plant to become self-compatible. We have now characterized two glycoproteins present in the styles of self-compatible and self-incompatible accessions of L. peruvianum: one is a ribonuclease that cosegregates with a functional self-incompatibility allele (S6 allele); the other cosegregates with the self-compatible allele (S, allele) but has no ribonuclease activity. The derived amino acid sequences of the cDNAs encoding the S6 and Sc glycoproteins resemble sequences of other ribonucleass encoded by the S locus. The derived sequence for the S. glycoprotein differs from the others by lacking one of the hidine residues found in all other S-locus ribonucleases. These findings demonstrate the essential role of ribonuclease activity in self-incompatibility and lend further weight to evidence that this hisidine residue is involved in the catalytic site of the enzyme.Self-incompatibility is a major factor affecting mating systems in flowering plants (1, 2). In plants with gametophytic self-incompatibility such as members of the Solanaceae, rejection or acceptance of pollen tubes by the style is controlled by a single, multiallelic locus, the S locus. Pollen expresses its haploid S genotype, and matings are incompatible if the S allele of the pollen is matched by one of the two alleles expressed in the pistil. Thus, self-incompatibility is an example of recognition between plant cells; the underlying mechanism may be similar to other recognition systems in plants such as those involved in host-pathogen interactions (3, 4). The products of the S locus are a class of extracellular glycoproteins with RNase activity called S-RNases (5, 6). The genes that encode these proteins cosegregate with alleles of the S locus (7, 8). S-RNases are abundant proteins found in high concentrations in the transmitting tract of the style, the site at which inhibition of pollen tubes occurs during incompatible matings (9). Sequences of S-RNase alleles from different solanaceous species share a characteristic structure that includes five short stretches of highly conserved sequence (10). Two of these conserved regions correspond to the sequences surrounding the catalytic domains of fungal RNases and include both of the histidine residues essential for catalytic activity (11 LA2157 is self-compatible and has S genotype SS,; LA2163 is self-incompatible and has the S genotype 56S7 (16). L. peruvianum plants homozygous for the S6 allele were produced by self-pollinating heterozygous individuals at the green bud stage as described (16).Purification and N-Terminal Sequencing of the S6 and S, Glycoproteins. Extracts from 50 styles of plants homozygous for the S6 or S, alleles were prepared and fractionated by cation-exchange chromatography as described (18). S glycoproteins recovered from the extract after ammonium...

Iron is an essential element for most living organisms, and pathogens are likely to compete with their hosts for the acquisition of this element. The bacterial plant pathogen Dickeya dadantii has been shown to require its siderophore-mediated iron uptake system for systemic disease progression on several host plants, including Arabidopsis thaliana. In this study, we investigated the effect of the iron status of Arabidopsis on the severity of disease caused by D. dadantii. We showed that symptom severity, bacterial fitness and the expression of bacterial pectate lyase-encoding genes were reduced in iron-deficient plants. Reduced symptoms correlated with enhanced expression of the salicylic acid defence plant marker gene PR1. However, levels of the ferritin coding transcript AtFER1, callose deposition and production of reactive oxygen species were reduced in iron-deficient infected plants, ruling out the involvement of these defences in the limitation of disease caused by D. dadantii. Disease reduction in iron-starved plants was also observed with the necrotrophic fungus Botrytis cinerea. Our data demonstrate that the plant nutritional iron status can control the outcome of an infection by acting on both the pathogen's virulence and the host's defence. In addition, iron nutrition strongly affects the disease caused by two soft rot-causing plant pathogens with a large host range. Thus, it may be of interest to take into account the plant iron status when there is a need to control disease without compromising crop quality and yield in economically important plant species.