Submitted to: Physiological and Molecular Plant Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/29/2004
Publication Date: N/A
Citation: N/A Interpretive Summary: Several species of fungal pathogens produce toxic metabolites that account for their ability to cause plant disease. However, the timing of the production and secretion of such toxins onto or into the host plant have not been documented. With sensitive analytical methods, we detected the presence of HC-toxin, produced by the corn leaf pathogen Cochliobolus carbonum, on the surface of leaves of a resistant plant prior to penetration of the leaf. Nevertheless, the resistant plant was able to rapidly degrade the toxin before it exerted its toxic effects, suggesting that the plant had the ability to inactivate the toxin at a very early stage in the infection process. The results will contribute to the body of knowledge concerning the mechanisms by which plants avoid damage caused by fungal pathogens and will be useful to plant pathologists and plant biologists studying disease resistance.
Technical Abstract: Conidia of the maize pathogen Cochliobolus carbonum secrete the host-selective toxin known as HC-toxin during formation of appressoria on the surface of resistant maize leaves. Plasma desorption mass spectrometry revealed that approximately 70 ng of toxin per 106 conidia were secreted during the first 16 h of morphogenesis on the leaf surface. Growth of the fungus over time in resistant and susceptible isogenic maize lines was monitored microscopically by staining with Calcofluor. Extensive growth of the fungus in the susceptible disease interaction occurred as early as 24 h post-inoculation. In contrast, in spite of the presence of a substantial amount of HC-toxin in the resistant interaction, the fungus failed to become established in the host even after 36 h. The results suggest that the Hm1 resistance gene is either expressed constitutively or in response to the presence of the HC-toxin. In either case, the HC-toxin is inactivated early in the disease interaction.