Tomato protein kinase 1b mediates signaling of plant responses to necrotrophic fungi and insect herbivory
Tomato protein kinase 1b mediates signaling of plant responses to necrotrophic fungi and insect herbivory
复制标题
DOI：
10.1105/tpc.108.059477
复制
发表时间：
2008-07-01
期刊：
影响因子：
11.6
通讯作者：
Mengiste, Tesfaye
中科院分区：
文献类型：
--
作者：
AbuQamar, Synan;Chai, Mao-Feng;Mengiste, Tesfaye
番茄蛋白激酶 1 (TPK1b) 基因编码一种定位于质膜的受体样细胞质激酶。病原体感染、机械损伤和氧化应激会诱导 TPK1b 表达，通过 RNA 干扰 (RNAi) 降低 TPK1b 基因表达会增加番茄对坏死营养真菌灰葡萄孢 (Botrytis cinerea) 和烟草天蛾 (Manduca sexta) 幼虫摄食的敏感性，但不会增加对细菌病原体丁香假单胞菌 (Pseudomonas syringae) 的敏感性。 TPK1b RNAi 幼苗的乙烯 (ET) 反应也受到损害。值得注意的是，对灰霉病和昆虫摄食的易感性与蛋白酶抑制剂 II 基因响应灰霉病和 1-氨基环丙烷-1-羧酸（ET 的天然前体）表达减少相关，但野生型表达响应机械损伤和茉莉酸甲酯。 TPK1b 的功能独立于 JA 生物合成和抵抗灰霉病所需的反应基因。 TPK1b 是一种具有自磷酸化和髓磷脂基础蛋白磷酸化活性的功能性激酶。激活片段中的三个残基在 TPK1b 的激酶活性和体内信号传导功能中发挥着关键作用。总之，我们的研究结果确立了 TPK1b 在 ET 介导的共同防御机制中的信号作用，以抵抗死体营养真菌和草食性昆虫。
The tomato protein kinase 1 (TPK1b) gene encodes a receptor-like cytoplasmic kinase localized to the plasma membrane. Pathogen infection, mechanical wounding, and oxidative stress induce expression of TPK1b, and reducing TPK1b gene expression through RNA interference (RNAi) increases tomato susceptibility to the necrotrophic fungus Botrytis cinerea and to feeding by larvae of tobacco hornworm (Manduca sexta) but not to the bacterial pathogen Pseudomonas syringae. TPK1b RNAi seedlings are also impaired in ethylene (ET) responses. Notably, susceptibility to Botrytis and insect feeding is correlated with reduced expression of the proteinase inhibitor II gene in response to Botrytis and 1-aminocyclopropane-1-carboxylic acid, the natural precursor of ET, but wild-type expression in response to mechanical wounding and methyljasmonate. TPK1b functions independent of JA biosynthesis and response genes required for resistance to Botrytis. TPK1b is a functional kinase with autophosphorylation and Myelin Basis Protein phosphorylation activities. Three residues in the activation segment play a critical role in the kinase activity and in vivo signaling function of TPK1b. In sum, our findings establish a signaling role for TPK1b in an ET-mediated shared defense mechanism for resistance to necrotrophic fungi and herbivorous insects.