Laboratory of Phytopathology, Plant Sciences Group, Wageningen University, Wageningen, The Netherlands.
PLoS Pathog. 2011 Mar;7(3):e1001327. doi: 10.1371/journal.ppat.1001327. Epub 2011 Mar 31.
In plants, an active defense against biotrophic pathogens is dependent on a functional continuum between the cell wall (CW) and the plasma membrane (PM). It is thus anticipated that proteins maintaining this continuum also function in defense. The legume-like lectin receptor kinase LecRK-I.9 is a putative mediator of CW-PM adhesions in Arabidopsis and is known to bind in vitro to the Phytophthora infestans RXLR-dEER effector IPI-O via a RGD cell attachment motif present in IPI-O. Here we show that LecRK-I.9 is associated with the plasma membrane, and that two T-DNA insertions lines deficient in LecRK-I.9 (lecrk-I.9) have a 'gain-of-susceptibility' phenotype specifically towards the oomycete Phytophthora brassicae. Accordingly, overexpression of LecRK-I.9 leads to enhanced resistance to P. brassicae. A similar 'gain-of-susceptibility' phenotype was observed in transgenic Arabidopsis lines expressing ipiO (35S-ipiO1). This phenocopy behavior was also observed with respect to other defense-related functions; lecrk-I.9 and 35S-ipiO1 were both disturbed in pathogen- and MAMP-triggered callose deposition. By site-directed mutagenesis, we demonstrated that the RGD cell attachment motif in IPI-O is not only essential for disrupting the CW-PM adhesions, but also for disease suppression. These results suggest that destabilizing the CW-PM continuum is one of the tactics used by Phytophthora to promote infection. As countermeasure the host may want to strengthen CW-PM adhesions and the novel Phytophthora resistance component LecRK-I.9 seems to function in this process.
在植物中，对生物营养病原体的主动防御依赖于细胞壁 (CW) 和质膜 (PM) 之间的功能连续性。因此，可以预期维持这种连续性的蛋白质也在防御中发挥作用。类豆科植物凝集素受体激酶 LecRK-I.9 是拟南芥 CW-PM 黏附的假定介质，已知通过存在于 IPI-O 中的 RGD 细胞附着基序在体外与 Phytophthora infestans RXLR-dEER 效应物 IPI-O 结合。在这里，我们表明 LecRK-I.9 与质膜相关，并且两个 T-DNA 插入系 LecRK-I.9 缺陷（lecrk-I.9）对卵菌 Phytophthora brassicae 具有“易感性增加”表型。相应地，LecRK-I.9 的过表达导致对 P. brassicae 的增强抗性。在表达 ipiO（35S-ipiO1）的转基因拟南芥系中观察到类似的“易感性增加”表型。这种表型复制行为也观察到与其他防御相关功能有关；lecrk-I.9 和 35S-ipiO1 在病原体和 MAMP 触发的胼胝质沉积中均受到干扰。通过定点突变，我们证明了 IPI-O 中的 RGD 细胞附着基序不仅对于破坏 CW-PM 黏附是必需的，而且对于疾病抑制也是必需的。这些结果表明，破坏 CW-PM 连续性是 Phytophthora 促进感染的策略之一。作为对策，宿主可能希望加强 CW-PM 黏附，而新型 Phytophthora 抗性成分 LecRK-I.9 似乎在此过程中发挥作用。
