ETHYLENE ENHANCES THE ANTIFUNGAL LIPID CONTENT IN IDIOBLASTS FROM AVOCADO MESOCARP ALICIA LEIKIN-FRENKEL and DOV PRUSKY* Department of Postharvest Science of Fresh Produce, The Volcani Center, Bet Dagan 50250 Israel (Received in revised form 2 February 1998) Key Word Index—Persea americana; Lauraceae; Colletotrichum gloeosporioides; preformed compounds; fruit resistance to postharvest diseases; oil cells. Abstract—It has previously been demonstrated that exposure of whole avocado fruits cv. Fuerte to 40 ml/l ethylene for 3 hours enhances the level of antifungal 1-acetoxy-2-hydroxy-4-oxo-heneicosa-12, 15-diene (diene) in the fruit pericarp. Exposure of 1–2 mm slices of fruit pericarp and mesocarp to ethylene enhanced the level of the antifungal diene in the mesocarp only. Since most of the antifungal diene in the mesocarp is compartmentalized in idioblasts, the eect of ethylene was tested on isolated idioblasts. Exposure of idioblasts to ethylene increased the level of antifungal diene twofold within 3 hours. This eect was temperature dependent. Three hours exposure of idioblasts to ethylene at 358 doubled the diene content compared to less than 50% increase after three hours at 208. Incubation of idioblasts with [2- 14 C]malonyl-CoA or [1- 14 C]acetate in the presence of ethylene, showed the incorporation of the label into a compound that co-chromatographed with the antifungal diene. The compound induced by ethylene and released from the cells was identified by NMR as the antifungal diene. The present report suggests that ethylene can induce the synthesis of the antifungal diene in idioblasts and the export of this compound to the pericarp of the fruits. # 1998 Published by Elsevier Science Ltd. All rights reserved INTRODUCTION Colletotrichum gloeosporioides attacks avocado fruits during growth in the orchard. The pathogen germinates and penetrates unripe fruit but remains quiescent until harvesting [1]. After harvest, fruit ripening is accompanied by activation of fungal development and appearance of decay symptoms. Resistance of unripe fruit to postharvest pathogens is related to the presence of preformed antifungal compounds in fruit pericarp (peel). The most active of them was found to be an antifungal diene [2]. The level of this compound decreases during ripen- ing thus enabling the activation of the quiescent infections and symptom expression [1]. Metabolism of the antifungal diene and increased susceptibility after harvest is mediated by lipoxygenase. The ac- tivity of this enzyme is, in turn, regulated by the levels of a non-specific inhibitor in the pericarp identified as epicatechin whose levels decrease mark- edly in ripe fruits [1]. Enhanced levels of the antifungal diene caused by biotic and abiotic elicitors may depend on the bal- ance between rates of synthesis and breakdown of the compound [1]. Two possibilities exist for main- taining fungitoxic levels of antifungal compounds in the tissue of ripening fruits: (i) prevention of cata- bolism, (ii) induction of synthesis. Several biotic and abiotic elicitors that increased the levels of the antifungal diene also led to higher levels of epicatechin [3]. These results seem to imply that abiotic elicitors may enhance the levels of antifungal diene by inhibiting its catabolism. On the other hand, increase of antifungal diene may result from the induced synthesis of the compound. The syn- thesis of the antifungal diene may originate from acetate and malonate, like fatty acids, or be a sec- ondary product of lipid metabolism [4]. The location of the sites of biosynthesis of the antifungal compounds in avocado fruits has never been described. A previous report by Kobiler et al. [5] described the presence of antifungal com- pounds compartmentalized in specific oil cells in the mesocarp of avocado. Interestingly, about 85% of all antifungal compounds within the mesocarp were located in these cells which suggested the possibility that the synthesis of antifungal compounds may occur in specific idioblasts. In the present work we Phytochemistry Vol. 49, No. 8, pp. 2291–2298, 1998 # 1998 Published by Elsevier Science Ltd. All rights reserved Printed in Great Britain 0031-9422/98/$ - see front matter PII: S0031-9422(98)00147-2 *Author to whom correspondence should be addressed. 2291