Abstract

Abstract Fusarium oxysporum f. sp. cepae produced an exo‐polygalacturonase (exo‐PG) and endopectin‐trans‐eliminase (endo‐PTE) in a mineral medium supplemented with a restricted supply of either D‐galacturonic acid or onion cell walls. These enzymes were also extracted from infected onion tissue, but only endo‐PTE caused tissue maceration and cell death.The patterns of host tissue colonization and pectic enzyme production were followed during bulb rot development. Stem plates were invaded within two weeks of inoculation. The pathogen then remained confined to the stem plates for several weeks or months, before spreading to the outer fleshy scales to initiate a basal rot. In most cases the inner leaf sheaths containing the lateral bud remained healthy. Exo‐PG activity m stem plate tissue was greatest at two weeks after inoculation, then it declined. Endo‐PTE was not detected in newly invaded stem plate tissue, but was recovered from infected stem plates before decay and from the bases of bulb scales and leaf sheaths at the onset of bulb rot. There was no pectic enzyme activity in uninvaded onion tissue.Spread of the fungus and pectic enzyme production in two Caledon Globe genotypes susceptible or tolerant to F. oxysporum f. sp. cepae were similar, but the onset of bulb rot in tolerant genotypes was considerably delayed.

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