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辣椒对野油菜黄单胞菌辣椒斑点病致病变种过敏反应期间过氧化物酶样基因的表达、H2O2产生及过氧化物酶活性

Expression of peroxidase-like genes, H2O2 production, and peroxidase activity during the hypersensitive response to Xanthomonas campestris pv. vesicatoria in Capsicum annuum.

作者信息

Do Hyun Mee, Hong Jeum Kyu, Jung Ho Won, Kim Sang Hee, Ham Jong Hyun, Hwang Byung Kook

机构信息

Laboratory of Molecular Plant Pathology, College of Life and Environmental Sciences, Korea University, Seoul 136-701, Korea.

出版信息

Mol Plant Microbe Interact. 2003 Mar;16(3):196-205. doi: 10.1094/MPMI.2003.16.3.196.

Abstract

Pepper ascorbate peroxidase-like (CAPOA1), thioredoxin peroxidase-like (CAPOT1), and peroxidase-like (CAPO1) clones were isolated from pepper leaves inoculated with avirulent strain Bv5-4a of Xanthomonas campestris pv. vesicatoria. CAPOA1, CAPOT1, and CAPO1 mRNA disappeared 18 to 30 h after the bacterial infection when the hypersensitive response (HR) was visible. In contrast, peroxidase activity reached a peak at 18 h after infection and then declined at 24 and 30 h when H2O2 accumulation level was maximal. These results suggest that the striking accumulation of H2O2 and strong decrease in peroxidase activity during the programmed cell death may be due to the strong suppression of CAPOA1, CAPOT1, and CAPO1 gene expression. Infection by Phytophthora capsici or Colletotricum gloeosporioides also induced the expression of the three putative peroxidase genes in pepper tissues. CAPOA1 mRNAs were in situ localized in phloem areas of vascular bundles in pepper tissues infected by Colletotricum. coccodes, P. capsici, or C. gloeosporioides. Exogenous treatment with H2O2 strongly induced the CAPOA1 and CAPOT1 transcription 1 h after treatment, while the CAPO1 transcripts accumulated 12 h after H2O2 treatment. We suggest that pepper ascorbate peroxidase and thioredoxin peroxidase genes may function as regulators of H2O2 level and total peroxidase activity in the oxidative burst during the HR to incompatible pathogen interaction in pepper plant.

摘要

从接种了野油菜黄单胞菌辣椒致病变种无毒菌株Bv5 - 4a的辣椒叶片中分离出了抗坏血酸过氧化物酶样(CAPOA1)、硫氧还蛋白过氧化物酶样(CAPOT1)和过氧化物酶样(CAPO1)克隆。当可见过敏反应(HR)时,细菌感染后18至30小时,CAPOA1、CAPOT1和CAPO1 mRNA消失。相比之下,过氧化物酶活性在感染后18小时达到峰值,然后在24小时和30小时下降,此时过氧化氢(H₂O₂)积累水平最高。这些结果表明,在程序性细胞死亡期间H₂O₂的显著积累和过氧化物酶活性的强烈下降可能是由于CAPOA1、CAPOT1和CAPO1基因表达受到强烈抑制。辣椒疫霉或胶孢炭疽菌的感染也诱导了辣椒组织中这三个假定过氧化物酶基因的表达。在被球座炭疽菌、辣椒疫霉或胶孢炭疽菌感染的辣椒组织中,CAPOA1 mRNA原位定位于维管束的韧皮部区域。用H₂O₂进行外源处理1小时后强烈诱导CAPOA1和CAPOT1转录,而CAPO1转录本在H₂O₂处理12小时后积累。我们认为,辣椒抗坏血酸过氧化物酶和硫氧还蛋白过氧化物酶基因可能在辣椒植株与不亲和病原体相互作用的HR过程中的氧化爆发中作为H₂O₂水平和总过氧化物酶活性的调节因子发挥作用。

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