Features of the rapid cell death induced in cowpea by the monokaryon of the cowpea rust fungus or the monokaryon-derived cultivar-specific elicitor of necrosis

Abstract

Rapid cell death induced in the resistant cowpea cultivar, Dixie Cream, by the monokaryotic stage of race 1 of the cowpea rust fungus was delayed by treatments with Superoxide dismutase, mannitol, catalase and the lipoxygenase inhibitor salicyl hydroxamic acid. These treatments also delayed cell death caused by a cultivar-specific elicitor of necrosis present in intercellular washing fluids from monokaryon-infectcd susceptible plants. The data suggest that active oxygen species, hydrogen peroxide and lipid peroxidation may be involved in both elicitor- and fungal-induced cell death, and in both cases, treatments were effective when applied close to the onset of the first cytological signs of necrosis. Pre-inoculation treatment of cv. Dixie Cream with heat, or prenecrosis treatments with the protein synthesis inhibitor blasticidin S or abscisic acid, also delayed fungal-induced cell death, but heat was the only treatment of all those tested that resulted in a slight increase in fungal growth. Cell death was also delayed by damaging or killing the fungus at various stages before the normal onset of necrosis suggesting the necessity for sustained fungal metabolism. All of these data, and the time-course of elicitor-induced necrosis, are consistent with the hypothesis that the elicitor is the primary cause of cell death in this incompatible plant-fungal interaction. However, the data also suggest that cell death may not be the primary cause of the cessation of fungal growth.