Choi D, Bostock R M, Avdiushko S, Hildebrand D F
Department of Plant Pathology, University of California, Davis, CA 95616, USA.
Proc Natl Acad Sci U S A. 1994 Mar 15;91(6):2329-33. doi: 10.1073/pnas.91.6.2329.
Induction of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR; EC 1.1.1.34) is essential for the synthesis of steroid derivatives and sesquiterpenoid phytoalexins in solanaceous plants following mechanical injury or pathogen infection. Gene-specific probes corresponding to different HMGR genes (hmg1 and hmg2) were used to study HMGR expression in potato tissue following treatment with methyl jasmonate, a lipoxygenase product of linolenic acid, or arachidonic acid, an elicitor present in the lipids of the potato late blight fungus Phytophthora infestans. Treatment of potato discs (2.2 cm in diameter) with low concentrations (0.45-45 nmol per disc surface) of methyl jasmonate nearly doubled the wound-induced accumulation of hmg1 transcripts and steroid-glycoalkaloid (SGA) accumulation, reduced the abundance of hmg2 transcripts, and did not induce phytoalexins. High concentrations of methyl jasmonate (2-4.5 mol per disc surface) suppressed hmg1 mRNA and SGA accumulation but did not affect hmg2 mRNA abundance or induce phytoalexins. In contrast, arachidonate treatment strongly suppressed hmg1 and strongly induced hmg2 mRNA in a concentration-dependent manner. There was a corresponding suppression of SGA accumulation and an induction of sesquiterpene phytoalexin accumulation by this elicitor. Lipoxygenase inhibitors reduced the wound-induced accumulation of hmg1 transcripts and suppressed SGA levels, effects that were overcome by exogenous methyl 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 consistent with placement of the HMGR activities encoded by hmg1 and hmg2 within discrete steroid and sesquiterpenoid biosynthetic channels.
在茄科植物受到机械损伤或病原体感染后，诱导3-羟基-3-甲基戊二酰辅酶A还原酶（HMGR；EC 1.1.1.34）对于甾体衍生物和倍半萜类植物抗毒素的合成至关重要。使用与不同HMGR基因（hmg1和hmg2）对应的基因特异性探针，研究了用茉莉酸甲酯（亚麻酸的脂氧合酶产物）或花生四烯酸（马铃薯晚疫病菌致病疫霉脂质中的一种激发子）处理后马铃薯组织中HMGR的表达情况。用低浓度（每片表面0.45 - 45 nmol）的茉莉酸甲酯处理马铃薯圆盘（直径2.2 cm），使伤口诱导的hmg1转录本积累和甾体糖苷生物碱（SGA）积累几乎增加了一倍，降低了hmg2转录本的丰度，且未诱导植物抗毒素的产生。高浓度的茉莉酸甲酯（每片表面2 - 4.5 μmol）抑制了hmg1 mRNA和SGA积累，但不影响hmg2 mRNA丰度，也不诱导植物抗毒素。相反，花生四烯酸处理以浓度依赖的方式强烈抑制hmg1并强烈诱导hmg2 mRNA。这种激发子相应地抑制了SGA积累并诱导了倍半萜植物抗毒素积累。脂氧合酶抑制剂降低了伤口诱导的hmg1转录本积累并抑制了SGA水平，外源性茉莉酸甲酯（每片表面45 nmol）可克服这些影响。结果表明：（i）茉莉酸甲酯可作为受伤后hmg1表达和SGA诱导的信号；（ii）表明花生四烯酸和茉莉酸响应途径在HMGR基因表达和类异戊二烯产物积累方面是不同的。结果还与hmg1和hmg2编码的HMGR活性在不同的甾体和倍半萜生物合成途径中的定位一致。
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