Balagué Claudine, Gouget Anne, Bouchez Olivier, Souriac Camille, Haget Nathalie, Boutet-Mercey Stéphanie, Govers Francine, Roby Dominique, Canut Hervé
CNRS, Laboratoire des Interactions Plantes Microorganismes (LIPM), UMR2594, Castanet-Tolosan, 31326, France.
INRA, Laboratoire des Interactions Plantes Microorganismes (LIPM), UMR441, Castanet-Tolosan, 31326, France.
Mol Plant Pathol. 2017 Sep;18(7):937-948. doi: 10.1111/mpp.12457. Epub 2016 Sep 15.
On microbial attack, plants can detect invaders and activate plant innate immunity. For the detection of pathogen molecules or cell wall damage, plants employ receptors that trigger the activation of defence responses. Cell surface proteins that belong to large families of lectin receptor kinases are candidates to function as immune receptors. Here, the function of LecRK-I.9 (At5g60300), a legume-type lectin receptor kinase involved in cell wall-plasma membrane contacts and in extracellular ATP (eATP) perception, was studied through biochemical, gene expression and reverse genetics approaches. In Arabidopsis thaliana, LecRK-I.9 expression is rapidly, highly and locally induced on inoculation with avirulent strains of Pseudomonas syringae pv. tomato (Pst). Two allelic lecrk-I.9 knock-out mutants showed decreased resistance to Pst. Conversely, over-expression of LecRK-I.9 led to increased resistance to Pst. The analysis of defence gene expression suggests an alteration of both the salicylic acid (SA) and jasmonic acid (JA) signalling pathways. In particular, LecRK-I.9 expression during plant-pathogen interaction was dependent on COI1 (CORONATINE INSENSITIVE 1) and JAR1 (JASMONATE RESISTANT 1) components, and JA-responsive transcription factors (TFs) showed altered levels of expression in plants over-expressing LecRK-I.9. A similar misregulation of these TFs was obtained by JA treatment. This study identified LecRK-I.9 as necessary for full resistance to Pst and demonstrated its involvement in the control of defence against pathogens through a regulation of JA signalling components. The role of LecRK-I.9 is discussed with regard to the potential molecular mechanisms linking JA signalling to cell wall damage and/or eATP perception.
受到微生物攻击时，植物能够检测到入侵者并激活植物固有免疫。为了检测病原体分子或细胞壁损伤，植物利用受体来触发防御反应的激活。属于凝集素受体激酶大家族的细胞表面蛋白是作为免疫受体发挥功能的候选者。在此，通过生化、基因表达和反向遗传学方法研究了LecRK-I.9（At5g60300）的功能，LecRK-I.9是一种豆科型凝集素受体激酶，参与细胞壁与质膜的接触以及细胞外ATP（eATP）的感知。在拟南芥中，接种丁香假单胞菌番茄致病变种（Pst）的无毒菌株后，LecRK-I.9的表达会迅速、高度且局部地被诱导。两个等位基因的lecrk-I.9敲除突变体对Pst的抗性降低。相反，LecRK-I.9的过表达导致对Pst的抗性增加。防御基因表达分析表明水杨酸（SA）和茉莉酸（JA）信号通路均发生了改变。特别是，植物与病原体相互作用期间LecRK-I.9的表达依赖于COI1（冠菌素不敏感1）和JAR1（茉莉酸抗性1）组分，并且在过表达LecRK-I.9的植物中，JA响应转录因子（TFs）的表达水平发生了改变。通过JA处理也获得了这些TFs的类似失调情况。本研究确定LecRK-I.9是对Pst产生完全抗性所必需的，并证明其通过调节JA信号组分参与对病原体防御的控制。关于将JA信号与细胞壁损伤和/or eATP感知联系起来的潜在分子机制，对LecRK-I.9的作用进行了讨论。
