Search

Botrytis cinerea, the causal agent of blight, rot, and gray mold on many plant species, secretes various endopolygalacturonases during all stages of infection. The expression pattern of the encoding genes (Bcpg 1-6) was studied on four hosts: tomato, broad bean, apple, and courgette (also known as zucchini). All gene family members are differentially expressed, depending on the stage of infection and the host. Bcpg1 is expressed in all tissues tested although differences in transcript levels occur. Bcpg2 expression is detected early in the infection of three of four plant tissues tested. Bcpg3 and Bcpg5 are expressed in apple fruit tissue, although probably as a result of different regulatory mechanisms. The expression patterns of Bcpg4 and 6 are in agreement with their inducibility by monogalacturonic acid. The pattern of Bcpg gene expression indicates that B. cinerea is equipped with a flexible enzymatic pectate degradation machinery. The studies pinpoint new targets for gene disruption studies.

Saponins are an important group of glycosylated natural products which are widely distributed in the plant kingdom.1 They have attracted considerable attention because of their effects (both beneficial and detrimental) on human health, and because of their diverse range of other biological properties.1–5 Saponins are also of considerable interest to plant pathologists because these molecules often exhibit potent antifungal activity, suggestive of a role in the protection of plants against attack by phytopathogenic fungi.6,7 Because saponins are often present in relatively high levels in healthy plants, they may be regarded as pre-formed antimicrobial agents, in contrast to phytoalexins, which are synthesized in response to pathogen attack.

The fungus Cladosprium fulvum is a biotrophic leaf pathogen of tomato. The fungus develops in the intercellular space without forming specialized feeding structures and does not affect the leaf tissue. The outcome of the C. fulvum-tomato interaction can be described by the gene-for-gene model. Failure of infection is expressed by a hypersensitive response. Two fungal proteins, ECP1 and ECP2, have been isolated and their corresponding genes have been cloned. In a compatible interaction including many physiological races ECP1 and ECP2 are highly produced and a role in pathogenicity is suggestive. The ecp1 gene shows some homology with tumor necrosis factor receptors (TNFRs) while the ecp2 gene shows no homology with sequences known in data bases. However, disruption of one of the two genes showed no reduced pathogenicity of the fungus. Two race-specific elicitors, AVR4 and AVR9, have been isolated and their corresponding genes have been cloned. The avirulence genes Avr4 and Avr9 are only present in C. fulvum avirulent on Cf-4 and Cf-9 cultivars, respectively. The expression of these two genes is, like the expression of the ecp genes, highly induced when the fungus grows in planta. Disruption of the Avr9 gene in wild type avirulent races leads to virulence on tomato genotypes carrying the complementary resistance gene Cf-9. A single base-pair change in the avirulence gene Avr4 leads to virulence on tomato genotypes carrying the Cf-4 resistance gene. Isolation, characterization and possible function of ECP1, ECP2, AVR4, and AVR9 will be discussed.

The ED50 values and resistance factors of 20 fungicides that all act as inhibitors of the C-14 demethylation of 24-methylenedihydrolanosterol were determined for one wild-type and four resistant strains of Ustilago avenae. All fungicides were cross-resistant to each other; however, the resistance factors varied considerably, ranging from 50 (triadimenol) to 2·2 (miconazole). A tentative structural requirement for low resistant factors was the presence of two phenyl rings separated from each other by at least three atoms. Labeling of lipids with [14C]acetate in the absence and presence of the inhibitors and subsequent sterol analysis revealed that the variable resistance factors were not related to the presence of a second target site. In spite of reported second modes of action of fenarimol, tebuconazole or miconazole, accumulation of C-14 sterol precursors in both sensitive and resistant isolates was necessary to accomplish growth inhibition.