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A novel pepper (Capsicum annuum) receptor-like kinase functions as a negative regulator of plant cell death via accumulation of superoxide anions

机译:一种新型的辣椒(辣椒)受体样激酶通过超氧阴离子的积累作为植物细胞死亡的负调节剂

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Plant receptor-like kinases belong to a large gene family. The Capsicum annuum receptor-like kinase 1 (CaRLK1) gene encodes a transmembrane protein with a cytoplasmic kinase domain and an extracellular domain. The CaRLK1 extracellular domain (ECD)-green fluorescent protein (GFP) fusion protein was targeted to the plasma membrane, and the kinase domain of the CaRLK1 protein exhibited autophosphorylation activity. CaRLK1 transcripts were more strongly induced in treatment with Xag8ra than in treatment with Xag8-13. Furthermore, infection with incompatible Xanthomonas campestris pv. vesicatoria race 3 induced expression of CaRLK1 more strongly than in the compatible interaction. Cell death caused by both a disease-forming and an HR-inducing pathogen was delayed in the CaRLK1-transgenic plants. Ectopic expression of CaRLK1 also induced transcripts of the lesion stimulating disease (LSD) gene, a negative regulator of cell death. Respiratory burst oxidase homolog (RBOH) genes were up-regulated in the transgenic plants compared with the wild type, as the concentration of the superoxide anion was increased. In contrast, the concentration of HO did not differ between the transgenic and wild-type plants. These results support the theory that the suppression of plant cell death by CaRLK1 is associated with consistent production of the superoxide anion and induction of the RBOH genes and the LSD gene, but not with the concentration of HO. Thus, CaRLK1 may be a receptor of an as yet unidentified pathogen molecular pattern and may function as a negative regulator of plant cell death.
机译:植物受体样激酶属于一个大的基因家族。辣椒花样受体样激酶1(CaRLK1)基因编码具有细胞质激酶结构域和细胞外结构域的跨膜蛋白。 CaRLK1细胞外域(ECD)-绿色荧光蛋白(GFP)融合蛋白被靶向质膜,并且CaRLK1蛋白的激酶域表现出自磷酸化活性。与用Xag8-13处理相比,用Xag8ra处理更能诱导CaRLK1转录本。此外,感染了不相容的野油菜黄单胞菌。与相容性相互作用相比,vesicatoria第3种族更强烈地诱导CaRLK1的表达。在CaRLK1转基因植物中,由疾病形成和HR诱导病原体引起的细胞死亡被延迟。 CaRLK1的异位表达还诱导了病灶刺激疾病(LSD)基因的转录本,该基因是细胞死亡的负调节剂。与野生型相比,转基因植物中的呼吸爆发氧化酶同源(RBOH)基因上调,因为超氧化物阴离子的浓度增加。相反,HO的浓度在转基因植物和野生型植物之间没有差异。这些结果支持以下理论:CaRLK1抑制植物细胞死亡与超氧阴离子的稳定产生以及RBOH基因和LSD基因的诱导有关,而与HO的浓度无关。因此,CaRLK1可能是尚未确定的病原体分子模式的受体,并可能充当植物细胞死亡的负调节剂。

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