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Metabolism of 6-pentyl-2-pyrone (6PP) added at rates up to 120 μg/mL to liquid Botrytis cinerea cultures produced the previously unreported compounds 3-(2-pyron-6-yl)propanoic acid and 5-(2-pyron-6-yl)pentanoic acid. Another metabolite was identified tentatively from its mass spectrum as either 5-(2-pyron-6-yl)pentanol or 5-(2-pyron-6-yl)pentan-2-ol. B. cinerea hyphae remained viable with 6PP at 200 μg/mL, but their growth was suppressed at this concentration. Pyrone-containing metabolites were not observed in all systems to which 6PP had been added, but were formed in both hyphal development and sporulating phases of growth. These metabolites were stable in the presence of actively growing B. cinerea cultures and did not appear to alter fungal growth. It is proposed that the changes to the alkyl side chain in the metabolites reduced their lipophilicity and ability to permeate cell membranes relative to the parent compound, thus reducing their toxicity to the fungus. Keywords: 6-Pentyl-2-pyrone; 3-(2-pyron-6-yl)propanoic acid; 5-(2-pyron-6-yl)pentanoic acid; 5-(2-pyron-6-yl)pentanol; Botrytis cinerea; fungal metabolism; toxicity; biotransformation

Biotransformation of the antifungal Trichoderma metabolite 6-n-pentyl-2H-pyran-2-one (6PAP) (1) by Botrytis cinerea generated the previously reported 3-(2-pyron-6-yl)propionic acid (2) and 5-(2-pyron-6-yl)pentanoic acid (3) and allowed the isolation and characterization of a previously tentatively assigned product as 5-(2-pyron-6-yl)pentan-2-ol (5), plus allowed isolation of a new transformation product identified as 5-(2-pyron-6-yl)pentanoic acid (4). The full NMR spectral assignments of these four compounds are presented here for the first time, including some corrections to assignments previously published for 6PAP. Information is also presented on the relative toxicity of 6PAP and its four biotransformation products to B. cinerea, which shows that the metabolism products have reduced toxicity to the pathogenic organism.

Salicylic acid (SA), 1‐aminocyclopropane‐1‐carboxylic acid (ACC) and DL‐β‐amino‐n‐butyric acid (BABA) were screened for the ability to induce phenylalanine ammonia lyase (PAL) activity in kiwifruit (Actinidia deliciosa‘Hayward’) leaves. SA (2 mM) was the most effective and induced a 10‐fold rise in PAL activity after 2 days compared with a four‐fold rise 5 days after ACC (0.5 mM) treatment. BABA was not an effective elicitor of PAL. SA was further tested, alongside a chlorinated analogue 4‐chlorosalicylic acid (4CSA), for the ability to control Sclerotinia sclerotiorum on kiwifruit leaves. Pretreatment with SA and 4CSA caused a reduction in the size of lesions arising from subsequent S. sclerotiorum infection. 4CSA was the more effective and reduced disease levels, relative to controls, by up to 85% on leaf discs and 78% on leaves on the vine. This compares with a 48% reduction by SA on both. Resistance to infection was not affected by washing treated leaf discs prior to inoculation or by delaying inoculation for up to 4 days following 4CSA application. SA and 4CSA were rapidly absorbed and metabolized by kiwifruit leaves and had no apparent phytotoxic effects at the concentrations used for disease control studies. It is proposed that SA and 4CSA operate through the induction of host resistance mechanisms.

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