Abstract
The herbicide glyphosate, an inhibitor of the shikimic acid pathway and aromatic amino acid biosynthesis in plants, reduced the potential of Phaseolus vulgaris to defend itself effectively against races of Colletotrichum lindemuthianum without changing the nature of the interaction phenotype. Glyphosate did not block or diminish the occurrence of the hypersensitive reaction (HR) per se which is characteristic of the incompatible P. vulgaris-C. lindemuthianum host-pathogen interaction. The accumulation of phytoalexins which accompanies the HR was partially suppressed. Glyphosate at its sites of application sometimes enabled infection hyphase to grow from hypersensitive cells. Consequently, a spreading lesion formed which resulted in the collapse of the plant. The occurrence of glyphosate-induced spreading lesions was increased by treatments (e.g. light exposure, removal of cotyledons) that presumably competed for or depleted phenylalanine reserves in the plant. Spreading lesions developed at high frequency at wound sites on inoculated, glyphosate-treated plants. The increased frequency of spreading lesions caused by wounding cannot be accounted for solely by the presumed effect of glyphosate on accumulation of phytoalexins. The data indicate that infection hyphase of C. lindemuthianum remain viable at HR sites on P. vulgaris, and additionally, that the HR itself is not responsible for containment of the pathogen. The results support the conclusion that phytoalexin accumulation is a major feature of HR and a determinant of resistance in this host-parasite system.
Published Version
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