Necrosis- and ethylene-inducing peptide from Fusarium oxysporum induces a complex cascade of transcripts associated with signal transduction and cell death in arabidopsis
Necrosis- and ethylene-inducing peptide from Fusarium oxysporum induces a complex cascade of transcripts associated with signal transduction and cell death in arabidopsis
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DOI：
10.1104/pp.106.076869
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发表时间：
2006-07-01
期刊：
影响因子：
7.4
通讯作者：
Bailey, Bryan A.
中科院分区：
文献类型：
--
作者：
Bae, Hanhong;Kim, Moon S.;Bailey, Bryan A.
用来自尖孢镰刀菌的坏死和乙烯诱导肽（Nep 1）处理拟南芥（Arabidopsis thaliana）抑制根和子叶生长并引发细胞死亡，从而产生坏死点。Nep 1样蛋白由不同的微生物产生，其中许多是植物病原体。根据免疫定位结果，Nep 1在植物中定位于细胞壁和细胞质。与对照相比，用Nep 1处理75分钟后，叶绿素a荧光（F685 nm/F730 nm）的比率显著降低。这表明光合作用的短期补偿是对细胞局部损伤的反应。分析的大多数水溶性代谢物的浓度降低6小时后的Nep 1处理的拟南芥幼苗，表明细胞膜的完整性已经失败。微阵列结果表明，短期处理与Nep 1改变了许多基因的表达编码蛋白pupillary定位于细胞器，特别是叶绿体和线粒体。Nep 1的短期处理诱导了参与活性氧产生、信号转导、乙烯生物合成、膜修饰、细胞凋亡和应激的多类基因。定量PCR用于确认定位于叶绿体，线粒体和质膜中的基因的诱导，以及响应于钙/钙调蛋白复合物，乙烯，茉莉酸，乙烯生物合成，WRKY和细胞死亡的基因。大多数Nep 1诱导的基因与一般的胁迫反应有关，但与植物抗病性没有密切联系。这些结果与Nep 1促进细胞死亡作为由坏死营养型植物病原体引起的疾病的组成部分是一致的。
Treatment of Arabidopsis (Arabidopsis thaliana) with a necrosis- and ethylene-inducing peptide (Nep1) from Fusarium oxysporum inhibited both root and cotyledon growth and triggered cell death, thereby generating necrotic spots. Nep1-like proteins are produced by divergent microbes, many of which are plant pathogens. Nep1 in the plant was localized to the cell wall and cytosol based on immunolocalization results. The ratio of chlorophyll a fluorescence (F685 nm/F730 nm) significantly decreased after 75-min treatment with Nep1 in comparison to the control. This suggested that a short-term compensation of photosynthesis occurred in response to localized damage to cells. The concentrations of most water-soluble metabolites analyzed were reduced in Arabidopsis seedlings after 6 h of Nep1 treatment, indicating that the integrity of cellular membranes had failed. Microarray results showed that short-term treatment with Nep1 altered expression of numerous genes encoding proteins putatively localized to organelles, especially the chloroplast and mitochondria. Short-term treatment with Nep1 induced multiple classes of genes involved in reactive oxygen species production, signal transduction, ethylene biosynthesis, membrane modification, apoptosis, and stress. Quantitative PCR was used to confirm the induction of genes localized in the chloroplast, mitochondria, and plasma membrane, and genes responsive to calcium/calmodulin complexes, ethylene, jasmonate, ethylene biosynthesis, WRKY, and cell death. The majority of Nep1-induced genes has been associated with general stress responses but has not been critically linked to resistance to plant disease. These results are consistent with Nep1 facilitating cell death as a component of diseases caused by necrotrophic plant pathogens.