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Physiological and Molecular Plant Pathology (1988) 33, 105-114

The toxic effect of arachidonic acid and other unsaturated fatty acids on potato tuber cells


Uniuersity of Vermont, Burlington, Vermont 05405, U.S.A . Acceptedfor publication ,January 1988)

It is well known that arachidonic acid can elicit the accumulation of terpenoidphytoalexins in potato tubers . Other unsaturated fatty acids, such as linoleic and linolenic acid, do not elicit the accumulation of potato phytoalexins . However, both linoleic acid and arachidonic acid were found to elicit a hypersensitive-like response in protoplasts similar to that elicited by cell wall components from the fungus Phytophthora infestans . We continued our investigations to determinewhether unsaturated fatty acids elicit hypersensitive cell death in potato tuber tissue . It was found that unsaturated fatty acids were toxic to tuber cells . Linoleic acid and arachidonic acid were able to elicit significant cell death, whereas the esterified forms of arachidonic acid did not . Salycyl hydroxamic acid, which significantly blocked phytoalexin accumulation, did not block the celldeath elicited by arachidonic acid . The data indicate that the toxic effect of arachidonic acid on potato tuber cells is unrelated to its ability to induce phytoalexin accumulation . The findings also indicate that protoplasts may still be useful in this host-pathogen interaction since both potato tuber cells and protoplasts react similarly to elicitor treatments .


In potato,resistance to the late blight fungus Phylophthora infestans is characterized, in part, by hypersensitive cell death (HCD) and the accumulation of phytoalexins [9, 25] . The rapid cell death that occurs after invasion by incompatible races can occur within 30 min, in some cases, or take up to 12 h [25] . Hypersensitive cell death has been shown to be an energy requiring event since metabolic inhibitorswere able to prevent or slow the hypersensitive cell death [12, 25] . It follows, therefore, that HCD is part of the active defence mechanism of the plant. Following HCD are several biochemical changes that together are thought to play a role in preventing disease . These include the accumulation of phytoalexins [9, 20, 26], lignin accumulation [4, 14], and changes in enzyme activities in theacetate-mevalonate pathway [17] including those for phytoalexin synthesis [24], ethylene and ethane formation [5], and the formation of active oxygen species [11] . In a susceptible (compatible) reaction, however, the infected cells do not die rapidly but instead live on, two or more days after infection [25] . The accumulation of phytoalexins in response to fungal infection follows a pattern similarto the elicitation of cell death . High levels of phytoalexins accumulate very soon
*Current address : Purdue University, Department of Medicinal Chemistry, West Lafayette, Indiana 47906, U .S .A . Abbreviations used in text : AA, arachidonic acid ; 2,4-DNP, 2,4-dinitrophenol ; EA, eicosapentaenoic acid ; HCD, hypersensitive cell death ; HmG-CoA, 3-hydroxy 3-methylglutaryl CoA ; HR,hypersensitive response ; LA, linoleic acid ; SHAM, salycyl hydroxamic acid . 0885-5765/88/040105+ 10 $03 .00/0 © 1988 Academic Press Limited


D . A . Davis and W . W . Currier

after infection with incompatible races of the fungus, but the same levels are not reached until only much later after infection with compatible races [25] . The compatible fungus, which prevents or avoids eliciting celldeath, is able to establish itself and extensively invade the potato tissue . Later, this can often lead to death of the plant . Therefore, it is possible that by preventing rapid cell death the compatible fungus can stop or slow the biochemical changes which are responsible for resistance . Evidence in favour of this view includes the isolation of glucans from compatible races which are able to...
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