LIPID-DERIVED SIGNALS THAT DISCRIMINATE WOUND-RESPONSIVE AND PATHOGEN-RESPONSIVE ISOPRENOID PATHWAYS IN PLANTS - METHYL JASMONATE AND THE FUNGAL ELICITOR ARACHIDONIC-ACID INDUCE DIFFERENT 3-HYDROXY-3-METHYLGLUTARYL-COENZYME-A REDUCTASE GENES AND ANTIMICROBIAL ISOPRENOIDS IN SOLANUM-TUBEROSUM L

Induction of 3-hydroxy-3-methylglutarylcoenzyme A reductase (HMGR; EC 1.1.1.34) is essential for the synthesis of steroid derivatives and se squiterpenoid phytoalexins in solanaceous plants following mechanical injury or pathogen infection. Gene-specific probes corresponding to di fferent HMGR genes (hmg1 and hmg2) were used to study HMGR expression in potato tissue following treatment with methyl jasmonate, a lipoxyge nase product of linolenic acid, or arachidonic acid, an elicitor prese nt in the lipids of the potato late blight fungus Phytophthora infesta ns. Treatment of potato discs (2.2 cm in diameter) with low concentrat ions (0.45-45 nmol per disc surface) of methyl jasmonate nearly double d the wound-induced accumulation of hmg1 transcripts and steroid-glyco alkaloid (SGA) accumulation, reduced the abundance of hmg2 transcripts , and did not induce phytoalexins. High concentrations of methyl jasmo nate (2-4.5 mu mol per disc surface) suppressed hmg1 mRNA and SGA accu mulation but did not affect hmg2 mRNA abundance or induce phytoalexins . In contrast, arachidonate treatment strongly suppressed hmg1 and str ongly induced hmg2 mRNA in a concentration-dependent manner. There was a corresponding suppression of SGA accumulation and an induction of s esquiterpene phytoalexin accumulation by this elicitor. Lipoxygenase i nhibitors reduced the wound-induced accumulation of hmg1 transcripts a nd suppressed SGA levels, effects that were overcome by exogenous meth yl jasmonate (45 nmol per disc surface). The results (i) suggest that methyl jasmonate can function as a signal for hmg1 expression and SGA induction following wounding and (ii) indicate that the arachidonate- and jasmonate-response pathways are distinct in relation to HMGR gene expression and isoprenoid product accumulation. The results also are c onsistent with placement of the HMGR activities encoded by hmg1 and hm g2 within discrete steroid and sesquiterpenoid biosynthetic channels.