Symptom expression in the lethal leaf spot (LLS) mutant of maize (Zea mays L.), a disease lesion mimic conditioned by the homozygous recessive lls gene, was investigated to assess the rate of lesion development and to compare the phenolic compounds that accumulate in affected LLS leaf tissue with those that accumulate in wild-type sib-plants inoculated with the fungus Cochliobolus heterostrophus. Several esters of phenylpropanoids, including caffeic acid and ferulic acid, accumulated during lesion development in both the LLS mutant and in lesions incited by C. heterostrophus. A p-coumaric acid ester accumulated in the LLS lesions during their development but was not detected in uninoculated LLS controls or in leaves inoculated with the fungus. Unlike typical lesions incited by fungal pathogens and unlike the lesions in other disease mimics of maize, the lesions in LLS plants did not become delimited and attain a finite size. Lesions in LLS plants expanded at increasing rates until no living tissue remained on the leaf blade. Thus, LLS lesions expanded regardless of the accumulation of phenylpropanoid derivatives that are associated with lesion delimitation in fungal-induced lesions. The data suggest that lesion termination signals or factors proposed to restrict lesion expansion in disease mimics are absent from LLS plants.
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