Dipartimento di Biologia e Biotecnologie C. Darwin, Istituto Pasteur-Fondazione Cenci Bolognetti, Sapienza Università di Roma, 00185 Rome, Italy.
Plant Physiol. 2011 Nov;157(3):1163-74. doi: 10.1104/pp.111.184663. Epub 2011 Aug 31.
α-1-4-Linked oligogalacturonides (OGs) derived from plant cell walls are a class of damage-associated molecular patterns and well-known elicitors of the plant immune response. Early transcript changes induced by OGs largely overlap those induced by flg22, a peptide derived from bacterial flagellin, a well-characterized microbe-associated molecular pattern, although responses diverge over time. OGs also regulate growth and development of plant cells and organs, due to an auxin-antagonistic activity. The molecular basis of this antagonism is still unknown. Here we show that, in Arabidopsis (Arabidopsis thaliana), OGs inhibit adventitious root formation induced by auxin in leaf explants as well as the expression of several auxin-responsive genes. Genetic, biochemical, and pharmacological experiments indicate that inhibition of auxin responses by OGs does not require ethylene, jasmonic acid, and salicylic acid signaling and is independent of RESPIRATORY BURST OXIDASE HOMOLOGUE D-mediated reactive oxygen species production. Free indole-3-acetic acid levels are not noticeably altered by OGs. Notably, OG- as well as flg22-auxin antagonism does not involve any of the following mechanisms: (1) stabilization of auxin-response repressors; (2) decreased levels of auxin receptor transcripts through the action of microRNAs. Our results suggest that OGs and flg22 antagonize auxin responses independently of Aux/Indole-3-Acetic Acid repressor stabilization and of posttranscriptional gene silencing.
α-1-4 连接的低聚半乳糖醛酸（OGs）来源于植物细胞壁，是一类损伤相关分子模式，也是植物免疫反应的著名激发子。OGs 诱导的早期转录变化与 flg22 诱导的变化大部分重叠，flg22 是一种源自细菌鞭毛蛋白的肽，是一种特征明确的微生物相关分子模式，尽管随着时间的推移，反应会出现分歧。OGs 还由于具有生长素拮抗活性而调节植物细胞和器官的生长和发育。这种拮抗作用的分子基础尚不清楚。在这里，我们表明，在拟南芥（Arabidopsis thaliana）中，OGs 抑制了叶外植体中生长素诱导的不定根形成以及几个生长素应答基因的表达。遗传、生化和药理学实验表明，OGs 对生长素反应的抑制不需要乙烯、茉莉酸和水杨酸信号，并且独立于 RESPIRATORY BURST OXIDASE HOMOLOGUE D 介导的活性氧产生。OGs 不会明显改变游离吲哚-3-乙酸的水平。值得注意的是，OG 和 flg22-生长素拮抗作用不涉及以下任何机制：（1）生长素反应抑制剂的稳定化；（2）通过 microRNA 作用降低生长素受体转录本的水平。我们的结果表明，OGs 和 flg22 独立于 Aux/Indole-3-Acetic Acid 抑制剂的稳定化和转录后基因沉默拮抗生长素反应。
