Sensitization of defense responses and activation of programmed cell death by a pathogen-induced receptor-like protein kinase in Arabidopsis
Sensitization of defense responses and activation of programmed cell death by a pathogen-induced receptor-like protein kinase in Arabidopsis
复制标题
DOI：
10.1023/b:plan.0000009265.72567.58
复制
发表时间：
2003-09-01
影响因子：
5.1
通讯作者：
Chen, ZX
中科院分区：
文献类型：
--
作者：
Chen, KG;Du, LQ;Chen, ZX
在寻找WRKY DNA结合转录因子的潜在靶基因的过程中，我们先前已经鉴定了四个病原诱导的拟南芥基因（CRK5，CRK6，CRK10和CRK11），它们编码在其胞外结构域中含有新的富含半胱氨酸的重复序列的受体样蛋白激酶（RLKs）。在本研究中，我们转化拟南芥植物与组成型CaMV 35S启动子或类固醇诱导型Gal4启动子控制下的RLK基因。CRK5的表达，而不是其他三个RLK基因，导致转基因植物的防御反应和叶片生长的显着改变。在含有35S：：CRK5构建体的转基因植物中，CRK5的显著升高和组成型表达与增强的叶片生长和增加的对细菌病原体假单胞菌的抗性相关。转基因植株的抗病性增强与病原菌侵染后PR1基因更快地诱导表达有关。在类固醇诱导型启动子控制下用CRK5转化的转基因植物中，在类固醇应用后以相对高的水平诱导转基因的表达，并且这种诱导的CRK5表达引发过敏反应样细胞死亡。诱导的CRK5表达也激活了npr1，ndr1和eds1突变体和转基因nahG植物中的细胞死亡，这些植物不能积累水杨酸。因此，新的RLK能够激活多种不同的防御反应，这取决于其在转基因植物中过表达的方式和/或水平。
During the search for potential target genes of WRKY DNA-binding transcription factors, we have previously identified four pathogen-induced Arabidopsis genes (CRK5, CRK6, CRK10 and CRK11) encoding receptor-like protein kinases (RLKs) containing novel cysteine-rich repeats in their extracellular domains. In the present study, we transformed Arabidopsis plants with the RLK genes under control of the constitutive CaMV 35S promoter or a steroid-inducible Gal4 promoter. Expression of CRK5, but not the three other RLK genes, resulted in significant alterations in defense responses and leaf growth in transgenic plants. In transgenic plants harboring the 35S:: CRK5 construct, significantly elevated and constitutive expression of CRK5 correlated with enhanced leaf growth and increased resistance to the bacterial pathogen Pseudomonas syringae. The enhanced disease resistance in the transgenic plants was associated with more rapidly induced expression of the PR1 gene after pathogen infection. In transgenic plants transformed with CRK5 under control of the steroid-inducible promoter, expression of the transgene was induced at relatively high levels after the steroid application and this induced expression of CRK5 triggered hypersensitive response-like cell death. Induced CRK5 expression also activated cell death in the npr1, ndr1 and eds1 mutants and in the transgenic nahG plants that fail to accumulate salicylic acid. Thus, the novel RLK is capable of activating multiple distinct defense responses depending on the manner and/or the levels of its over-expression in transgenic plants.