Abstract
Seedlings of resistant (Sr6) and susceptible (sr6) near-isogenic lines of wheat (Triticum aestivum L.) were inoculated with an avirulent (P6) race of stem rust (Puccinia graminis (Pers.) f.sp. tritici Eriks. & Henn.) and kept for 2 days at 26 °C where the Sr6 gene is ineffective, treated with blasticidin S, ethionine, polyoxin D, or buffer, and transferred to 19 °C where the Sr6 gene is normally effective. One and 2 days later, leaves were stained with Calcofluor and examined by fluorescence microscopy to detect autofluorescing necrotic host cells and Calcofluor-stained stem rust colonies.Blasticidin S was phytotoxic to wheat leaves at concentrations that had no effect on fungal growth during the first 2 days after treatment. At later stages, extensive host necrosis, resulting from the phytotoxicity of this antibiotic, inhibited rust development.Ethionine and polyoxin D strongly inhibited rust development at concentrations that were not phytotoxic. In genotypically resistant leaves treated with ethionine and polyoxin D there were fewer necrotic cells associated with stem rust colonies than in leaves treated with buffer. The spacial distribution of necrotic cells was consistent with the view that necrosis occurs only in cells newly invaded after the temperature was lowered to 19 °C.The observations do not support the concept that host-cell necrosis in the hypersensitive reaction conditioned by this gene results from the death of the fungus.
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