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  • Title: Changes in oxylipin synthesis after Phytophthora infestans infection of potato leaves do not correlate with resistance.
    Author: Fauconnier ML, Rojas-Beltran J, Dupuis B, Delaplace P, Frettinger P, Gosset V, du Jardin P.
    Journal: Plant Physiol Biochem; 2008; 46(8-9):823-31. PubMed ID: 18538577.
    Abstract:
    Oxylipins constitute a class of molecules notably involved in host-pathogen interactions. In the potato-Phytophthora infestans (Mont.) De Barry (P. infestans) relationships, the role of colneleic and colnelenic acids, two oxylipins resulting from the consecutive action of lipoxygenase (EC 1.13.11.12) and divinyl ether synthase (EC 1.-) on respectively linoleic and linolenic acids have been previously reported. In the present paper, five potato cultivars with contrasting resistance to P. infestans were submitted to infection. Lipoxygenase pathway response was studied at both transcriptional and metabolic levels. A Northern blot preliminary study revealed that lipoxygenase (lox1 and lox3) and divinyl ether synthase genes were clearly up-regulated 96h after leaf inoculation with P. infestans. Profiling of free and esterified oxylipins performed 24h, 48h, 72h and 96h after inoculation, showed that esterified oxylipins are mainly produced with 9-derivatives in higher concentrations (esterified forms of colnelenic acid, 9-hydroxy octadecatrienoic acid, 9-hydroperoxy octadecatrienoic acid). Oxylipin accumulation is undetectable 24h after infection, slightly detectable after 48h, reaching highest concentrations after 96h. Cultivars show slightly different oxylipin profiles but the concentration of individual oxylipins differs markedly 96h after infection. No correlation was found between P. infestans resistance levels and oxylipin synthesis rates or concentration. To assess local and systemic effects of colneleic acid application before P. infestans infection, Bintje cultivar was sprayed with colneleic acid 72h before inoculation. Both application modes (local and systemic) resulted in lipoxygenase pathway activation without affecting the resistance level to the pathogen.
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