Transcriptional Characteristics of Xa21-mediated Defense Responses in Rice
Transcriptional Characteristics of Xa21-mediated Defense Responses in Rice
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DOI：
10.1111/j.1744-7909.2011.01032.x
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发表时间：
2011-04-01
影响因子：
11.4
通讯作者：
Liu, Guozhen
中科院分区：
文献类型：
--
作者：
Gan, Qiang;Bai, Hui;Liu, Guozhen
细菌性枯萎病，由黄单胞菌属细菌致病型引起。稻瘟病（Xoo）是水稻上最具破坏性的细菌性病害。克隆的水稻基因Xa 21赋予对广谱Xoo小种的抗性。为了鉴定与Xa 21介导的免疫相关的基因，利用水稻全基因组寡核苷酸芯片分别在接种后0、4、8、24、72和120 h（hpi）的不相容互作和模拟处理之间或在4 hpi的不相容互作和相容互作之间分析水稻基因的表达。共鉴定出441个差异表达基因，命名为XDG（Xa 21介导的差异表达基因）。根据XDG的功能注释，将XDG分为14类，包括防御相关、信号传导、转录调节因子。大多数防御相关基因属于病程相关基因家族，在72和120 hpi时被显著诱导。有趣的是，大多数信号和转录调节基因在4和8 hpi下调，这表明细胞信号的负调控可能在Xa 21介导的防御反应中发挥作用。Xa 21-和其他R基因介导的防御系统之间的表达谱的比较揭示了有趣的共同反应。还讨论了具有代表性的XDG及其支持证据。
Bacterial blight, caused by Xanthomonas oryzae pv. oryzae (Xoo), is the most destructive bacterial disease of rice. The cloned rice gene Xa21 confers resistance to a broad spectrum of Xoo races. To identify genes involved in Xa21-mediated immunity, a whole-genome oligonucleotide microarray of rice was used to profile the expression of rice genes between incompatible interactions and mock treatments at 0, 4, 8, 24, 72 and 120 h post inoculation (hpi) or between incompatible and compatible interactions at 4 hpi, respectively. A total of 441 differentially expressed genes, designated as XDGs (Xa21 mediated differentially expressed genes), were identified. Based on their functional annotations, the XDGs were assigned to 14 categories, including defense-related, signaling, transcriptional regulators. Most of the defense-related genes belonged to the pathogenesis-related gene family, which was induced dramatically at 72 and 120 hpi. Interestingly, most signaling and transcriptional regulator genes were downregulated at 4 and 8 hpi, suggesting that negative regulation of cellular signaling may play a role in the Xa21-mediated defense response. Comparison of expression profiles between Xa21- and other R gene-mediated defense systems revealed interesting common responses. Representative XDGs with supporting evidences were also discussed.