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Cavity spot of carrots: Interactions between the host and pathogen, related to the cell wall
Author(s) -
ZAMSKI E.,
PERETZ I.
Publication year - 1995
Publication title -
annals of applied biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.677
H-Index - 80
eISSN - 1744-7348
pISSN - 0003-4746
DOI - 10.1111/j.1744-7348.1995.tb06648.x
Subject(s) - apoplast , biology , symplast , turgor pressure , inoculation , pythium , leaf spot , cell wall , phenylalanine ammonia lyase , pathogen , botany , middle lamella , lignin , pathosystem , microbiology and biotechnology , pectinase , horticulture , peroxidase , enzyme , biochemistry
Summary This study investigates the structural aspects of cavity spot pathogenesis. Different Pythium spp. isolated from infected carrots, apples and melons were cultured on agar in Petri dishes and used for inoculation of uninfected carrots. Only slow‐growing Pythium spp. (< 15 mm day ‐1 ), such as P. violae and P. sulcatum caused cavity spot lesions. It is suggested that slow‐growing species are able to penetrate, albeit slowly, into the plant tissue for 3 to 4 days before a hypersensitive reaction develops. Fast‐growing species, however, did not cause lesions. Based on ultrastructural observations, we suggest that the following sequence of events occurs between the plant and the pathogen: The fungus infects the walls and grows for several days, during which time small amounts of wall‐degrading enzymes are secreted. Phenylalanine ammonia lyase (PAL) activity and phenols increase linearly immediately upon inoculation. There was a lag phase of about 5 days before lignin began to increase linearly for about a month. Dissolution of wall components decreases the solute potential and water potential in the apoplast. Thus, water moves from the symplast into the apoplast, the turgor pressure gradually dissipates, and the cells shrink and eventually die.