Major signaling pathways modulate Arabidopsis glucosinolate accumulation and response to both phloem-feeding and chewing insects
Major signaling pathways modulate Arabidopsis glucosinolate accumulation and response to both phloem-feeding and chewing insects
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DOI：
10.1104/pp.104.053389
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发表时间：
2005-06-01
期刊：
影响因子：
7.4
通讯作者：
Schultz, JC
中科院分区：
文献类型：
--
作者：
Mewis, I;Appel, HM;Schultz, JC
植物对天敌的反应是由几个相互作用的信号系统协调的。突变体和外源信号应用的分子和遗传学研究表明，茉莉酸（JA）、水杨酸（SA）和乙烯（ET）介导的途径调节拟南芥（Arabidopsis thaliana）中部分防御表型的表达，但尚未将这些观察结果与植物对昆虫攻击的反应直接联系起来。我们比较了 4 周龄突变体和转基因拟南芥（哥伦比亚）植物莲座叶的芥子油苷 (GS) 谱，这些植物在这三种主要信号通路中受到损害，并表征了这些植物对两种韧皮部取食蚜虫（多食性桃蚜和专食性短芽菜）和一种多食性毛虫物种（甜菜夜蛾）取食的反应。阻断冠状素不敏感 (coi1) 中的 JA 信号传导和增强过敏反应样 (hrl1) 突变体中 SA 信号的抗病性表达，降低了组成型 GS 浓度，而阻断介导蛋白 npr1 突变体 (NPR) 中的 SA 信号传导则增加了组成型 GS 浓度。阻断 ET 信号传导（ET 抗性 [etr1]）或降低 SA 浓度（nahG 转基因）对组成型 GS 含量没有显着影响。我们发现昆虫取食导致 GS 积累增加，这需要功能性 NPR1 和 ETR1，但不需要 COI1 或 SA。昆虫摄食主要导致短链脂肪族甲基亚磺酰基 GS 的增加。相比之下，对外源 JA（昆虫攻击的常见实验替代物）的反应特征是吲哚基 GS 增加。昆虫的表现（以种群增加或体重增加来衡量）与 GS 水平呈负相关，但我们发现有证据表明其他 ET 调节因素也可能产生影响。植物对甜菜夜蛾（被其消耗）的抗性与昆虫生长无关，因为一些植物化学物质抑制生长，而另一些则抑制取食。这些主要信号通路调节拟南芥 GS 积累以及对韧皮部取食和咀嚼昆虫的反应，通常是拮抗的； NPR 似乎是这些互动的核心。我们的结果表明，外源信号应用和植物消耗测量可能无法提供植物对实际昆虫摄食反应的有用测量。
Plant responses to enemies are coordinated by several interacting signaling systems. Molecular and genetic studies with mutants and exogenous signal application suggest that jasmonate (JA)-, salicylate (SA)-, and ethylene (ET)- mediated pathways modulate expression of portions of the defense phenotype in Arabidopsis (Arabidopsis thaliana), but have not yet linked these observations directly with plant responses to insect attack. We compared the glucosinolate (GS) profiles of rosette leaves of 4-week-old mutant and transgenic Arabidopsis (Columbia) plants compromised in these three major signaling pathways, and characterized responses by those plants to feeding by two phloem-feeding aphids (generalist Myzus persicae and specialist Brevicoryne brassicae) and one generalist caterpillar species (Spodoptera exigua Hubner). Blocked JA signaling in coronatine-insensitive (coi1) and enhanced expression of SA-signaled disease resistance in hypersensitive response-like (hrl1) mutants reduced constitutive GS concentrations, while blocking SA signaling at the mediator protein npr1 mutant (NPR) increased them. There was no significant impact on constitutive GS contents of blocking ET signaling (at ET resistant [etr1]) or reducing SA concentrations (nahG transgene). We found increased GS accumulation in response to insect feeding, which required functional NPR1 and ETR1 but not COI1 or SA. Insect feeding caused increases primarily in short-chain aliphatic methylsulfinyl GS. By contrast, responses to exogenous JA, a frequent experimental surrogate for insect attack, were characterized by an increase in indolyl GS. Insect performance, measured as population increase or weight increase, was negatively related to GS levels, but we found evidence that other, ET-regulated factors may also be influential. Plant resistance to (consumption by) S. exigua was not related to insect growth because some plant chemistries inhibited growth while others inhibited feeding. These major signaling pathways modulate Arabidopsis GS accumulation and response to both phloem-feeding and chewing insects, often antagonistically; NPR appears to be central to these interactions. Our results indicate that exogenous signal application and plant consumption measures may not provide useful measures of plant responses to actual insect feeding.