Abstract
An investigation was made of the mechanism by which the compounds 4,5-dihydro-4-methyltetrazolo[1,5- a]quinazolin-5-one (pp389); tricyclazole; and pyroquilon protect Phaseolus vulgaris from infection by the fungus Colletotrichum lindemuthianum. These compounds prevented infection of unwounded plant tissue, but not of tissue with a punctured epidermis. The compounds were not toxic to the pathogen at concentrations which blocked appressorial melanization and penetration of epidermal cell walls of bean and Bryophyllum. The compounds greatly increased the frequency of appressoria that produced non-penetrating hyphae which grew laterally along the epidermal surface. Control appressoria (52%) penetrated Formvar (polyvinyl formal) plastic membranes 100–140 nm thick, while only 2% of those treated with 10 μg ml −1 tricyclazole penetrated the membranes. The walls of untreated appressoria contained an electron-dense layer that was absent from walls of appressoria treated with pp389. The electron density of this layer increased in the region surrounding the infection pore. The basal part of untreated appressoria was conical in shape and focused on a relatively small area of the cuticle. Treated appressoria were poorly focused with a large flat basal area in contact with the cuticle. This study suggests that the unmelanized walls of treated appressoria lack the rigidity necessary to support the mechanical forces required for penetrating the plant cuticle.
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