An Arabidopsis (malectin-like) leucine-rich repeat receptor-like kinase contributes to downy mildew disease
An Arabidopsis (malectin-like) leucine-rich repeat receptor-like kinase contributes to downy mildew disease
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DOI：
10.1111/j.1365-3040.2011.02390.x
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发表时间：
2011-11-01
影响因子：
7.3
通讯作者：
Keller, Harald
中科院分区：
文献类型：
--
作者：
Hok, Sophie;Danchin, Etienne G. J.;Keller, Harald
生物营养型丝状植物病原体经常通过称为吸器的细胞内进食结构与宿主细胞建立密切接触。为了形成和维持这些结构，病原体必须避免或抑制防御反应并重新编程宿主细胞。我们使用拟南芥全基因组微阵列来表征在被活体营养型卵菌霜霉病病原体阿拉伯透明霜霉病菌感染期间被解除调控的遗传程序。在感染的早期和晚期观察到显著差异，但编码推定的富含亮氨酸重复序列受体样激酶（LRR-RLK）的基因不断上调。我们研究了这个基因的进化历史，注意到它是第一个从一个共同的祖先基因中出现的基因之一，通过复制产生了一组11个基因。编码的LRR-RLKs除了富含亮氨酸的短重复序列外，还含有细胞外的malectin-like（ML）结构域，因此与共生受体样激酶家族的蛋白质相似。详细的表达分析表明，病原体响应基因在卵菌周围的细胞中局部表达。一个敲除突变体表现出减少霜霉病感染，但通过突变互补的易感性完全恢复，这表明（ML-）LRR-RLK有助于疾病。根据突变表型，我们将其命名为受损的卵菌易感性1（IOS 1）。
Biotrophic filamentous plant pathogens frequently establish intimate contact with host cells through intracellular feeding structures called haustoria. To form and maintain these structures, pathogens must avoid or suppress defence responses and reprogramme the host cell. We used Arabidopsis whole-genome microarrays to characterize genetic programmes that are deregulated during infection by the biotrophic' oomycete downy mildew pathogen, Hyaloperonospora arabidopsidis. Marked differences were observed between early and late stages of infection, but a gene encoding a putative leucine-rich repeat receptor-like kinase (LRR-RLK) was constantly up-regulated. We investigated the evolutionary history of this gene and noticed it being one of the first to have emerged from a common ancestral gene that gave rise to a cluster of 11 genes through duplications. The encoded LRR-RLKs harbour an extracellular malectin-like (ML) domain in addition to a short stretch of leucine-rich repeats, and are thus similar to proteins from the symbiosis receptor-like kinase family. Detailed expression analysis showed that the pathogen-responsive gene was locally expressed in cells surrounding the oomycete. A knockout mutant showed reduced downy mildew infection, but susceptibility was fully restored through complementation of the mutation, suggesting that the (ML-) LRR-RLK contributes to disease. According to the mutant phenotype, we denominated it Impaired Oomycete Susceptibility 1 (IOS1).