A mandelamide pesticide alters lipid metabolism in Phytophthora infestans

Abstract

Summary• Several pesticide classes have been used for control of the notorious plant pathogen, Phytophthora infestans . Some of these alter lipids, suggesting that lipid metabolism may be a target site. Here, we investigate the action of a new, active, mandelamide compound, SX 623509 ( N -2 ′ -(4 ′′ -ethoxy-3 ′′ -methoxy) phenylethyl-3, 4-dichloromandelamide), on lipid metabolism.• Phytophthora infestans cultured in pea-broth or minimal media was exposed to different concentrations of SX 623509. Lipid metabolism was followed with radiolabelled acetate, choline or ethanolamine. Products were analysed following separation by thin-layer chromatography and gas-liquid chromatography.• SX 623509 reduced growth and lipid labelling from [ 14 C]acetate in both media. The inhibition in lipid labelling was not caused merely by a reduction in uptake of the radiolabelled precursor. There were changes in labelling patterns, particularly reductions in phosphatidylcholine and triacylglycerol and increases in phosphatidate and diacylglycerol. The effect of SX 623509 on phosphatidylcholine labelling was followed in more detail.• We conclude that the mandelamide pesticide SX 623509 reduces lipid synthesis at concentrations similar to those inhibiting growth. Specific effects on lipid labelling patterns are probably caused by inhibition of cholinephosphotransferase, which may be a future target site for pesticide development.

Field efficacy of mandipropamid for the control of potato late blight

“…(Huggenberger et al, 2005;Cohen et al, 2007). Together with dimethomorph, flumorph, iprovalicarb and benthiavalicarb, it was classified into one group of carbixylic acid amide (CAA) fungicides, mainly because filed isolates of Plasmopara viticola, showed cross-resistance to all the members of the group (FRAC, 2005;Cohen et al, 2007;Gisi et al, 2007).…”

“…The mode of action of CAA fungicides is not known. Biochemical studies with the mandelamide compound SX 623509 in mycelium of P. infestans suggested alternations in phospholipid biosynthesis, with inhibition of phosphatidylcholine (lecithin) biosynthesis as the main target (Griffiths at al., 2003;Cohen et al, 2007). The suggested inhibited enzyme was phosphocholinetransferase, the last enzyme in the Kennedy pathway (Griffiths at al., 2003;Cohen et al, 2007).…”

“…It is also an inhibitor of mycelial growth and sporulation (Huggenberger et al, 2005). Being rapidly adsorbed to the wax layer of the plant surface, mandipropamid provides a rainfast and longlasting barrier to fungal diseases (Lamberth et al, 2008).…”

Fungicide modes of action and resistance in downy mildews

“…The biochemical mode of action of CAA fungicides (including dimethomorph, flumorph, iprovalicarb, benthiavalicarb, mandipropamid) is still speculative; potential targets are phospholipid biosynthesis (Griffiths et al 2003) and cell wall deposition (Jende et al 2002;Gisi et al 2007a). Although CAAs may interfere with cell membranes, it is doubtful whether the observed effects on phosphocholinetransferase, the last step in the Kennedy pathway of lecithin biosynthesis (Griffiths et al 2003) can be considered as primary effects caused by CAA fungicides.…”

“…Although CAAs may interfere with cell membranes, it is doubtful whether the observed effects on phosphocholinetransferase, the last step in the Kennedy pathway of lecithin biosynthesis (Griffiths et al 2003) can be considered as primary effects caused by CAA fungicides. Similarly, the observed changes in cell wall architecture and deposition during germination of cystospores (Jende et al 2002) may be a secondary effect, because some of the key enzymes of cell wall biosynthesis such as glucanases and synthases of β-1,3 glucans and cellulose may not be inhibited directly (Mehl and Buchenauer 2002;Gisi et al 2007a).…”