一个阿罗酸脱水酶调控拟南芥对白粉病的抗性及盐胁迫响应

An Arogenate Dehydratase Regulates Powdery Mildew Resistance and Salt Response in Arabidopsis

摘要: 白粉病是一种具有广泛宿主的病害，每年给农业生产造成巨大损失。植物对白粉病的抗性主要由水杨酸途径介导，而水杨酸途径的激活常伴随严重的生长缺陷及作物减产。拟南芥pmr5突变体是一个不依赖于水杨酸途径的抗白粉病突变体，pmr5，ps8为其回复突变体，表现为感病表型。为了解析pmr5突变体抗病机制，寻找下游关键基因，我们采用传统图位克隆与全基因组测序辅助的图位克隆的方法克隆ps8突变，发现一个阿罗酸脱水酶ADT2 (Arogenate Dehydratase 2)的突变造成了pmr5;ps8的感病表型。前人报道ADT2作为苯丙氨酸合成途径的一个重要基因，调控植物对盐胁迫响应和花青素的积累等多个生物学过程。本研究首次发现ADT2也参与抗病调控。找到不依赖于水杨酸途径的抗白粉病关键基因，有助于培育不依赖于水杨酸途径的抗病作物，力争在抗病的前提下避免作物减产，同时培育多抗作物。

Abstract: Powdery mildew is a plant pathogen with a wide range of hosts, which causes great loss in agricultural production. Plant defense against powdery mildew is well known to be salicylic acid (SA)-dependent. However, activation of SA pathway is often accompanied by growth defect and yield penalty. Here we have an Arabidopsis mutant pmr5, which shows a perfect SA-independent powdery mildew resistant phenotype. To figure out the molecular mechanism of this defense and to find the key regulators in this pathway, we isolated a pmr5 suppressor, pmr5; ps8, in which a mutation in ps8 fully suppresses pmr5 resistance. By combining traditional map-based cloning and modern mapping-by-sequencing approaches, we found a mutation in ADT2 (Arogenate Dehydratase 2) is responsible for the pmr5; ps8 susceptible phenotype. ADT2, as a key regulator of phenoalanin bio-synthesis, is reported to be involved in salt stress response and anthocyanin accumulation. This is the first report of ADT2 involvement in pathogen defense. The finding of key regulators of SA-independent defense pathways can facilitate breeding of powdery mildew-resistant crops with-out yield loss. ADT2 also provides a possibility for breeding multiple-resistant crops.