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Dichloroisonicotinic and salicylic acid, inducers of systemic acquired resistance, enhance fungal elicitor responses in parsley cells
Author(s) -
Kauss Heinrich,
TheisingerHinkel Elke,
Mindermann Roswitha,
Conrath Uwe
Publication year - 1992
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.1992.tb00134.x
Subject(s) - elicitor , salicylic acid , systemic acquired resistance , phenylalanine ammonia lyase , inducer , biochemistry , coumarin , phenylalanine , endogeny , biology , secretion , enzyme , gene , amino acid , botany , arabidopsis , mutant
Certain plant species that were previously infected by pathogenic organisms subsequently develop a systemic resistance to further infection. This systemic acquired resistance can also be achieved by treatment with 2,6‐dichloroisonicotinic acid. Although this chemical does not directly induce coumarin secretion in suspension‐cultured cells of parsley ( Petroselinum crispum ), preincubation of the cultures with the compound greatly increases the subsequent induction of coumarin derivatives by a fungal elicitor, especially at low elicitor concentrations and in cell batches exhibiting a low response due to unknown variations in growth conditions. The effect appears to result from an increase in the sensitivity of the cells towards the elicitor, which causes enhanced transcription of genes coding for enzymes involved in coumarin synthesis. The enhanced transcriptional and translational activity is examplified by two specific mRNAs and the activity of phenylalanine ammonia lyase and S‐adenosyl‐ l ‐methionine:xantho‐toxol O‐methyl transferase. Salicylic acid, which has been implicated as an endogenous signal substance in systemic acquired resistance, causes similar but less pronounced effects. The results suggest that both acids may act by inducing increased synthesis of unknown components of the signal perception or transmission pathway which are rate‐limiting in untreated cells.