Brosché Mikael, Blomster Tiina, Salojärvi Jarkko, Cui Fuqiang, Sipari Nina, Leppälä Johanna, Lamminmäki Airi, Tomai Gloria, Narayanasamy Shaman, Reddy Ramesha A, Keinänen Markku, Overmyer Kirk, Kangasjärvi Jaakko
Division of Plant Biology, Department of Biosciences, University of Helsinki, Helsinki, Finland ; Institute of Technology, University of Tartu, Tartu, Estonia.
Division of Plant Biology, Department of Biosciences, University of Helsinki, Helsinki, Finland.
PLoS Genet. 2014 Feb 13;10(2):e1004112. doi: 10.1371/journal.pgen.1004112. eCollection 2014 Feb.
Plant responses to changes in environmental conditions are mediated by a network of signaling events leading to downstream responses, including changes in gene expression and activation of cell death programs. Arabidopsis thaliana RADICAL-INDUCED CELL DEATH1 (RCD1) has been proposed to regulate plant stress responses by protein-protein interactions with transcription factors. Furthermore, the rcd1 mutant has defective control of cell death in response to apoplastic reactive oxygen species (ROS). Combining transcriptomic and functional genomics approaches we first used microarray analysis in a time series to study changes in gene expression after apoplastic ROS treatment in rcd1. To identify a core set of cell death regulated genes, RCD1-regulated genes were clustered together with other array experiments from plants undergoing cell death or treated with various pathogens, plant hormones or other chemicals. Subsequently, selected rcd1 double mutants were constructed to further define the genetic requirements for the execution of apoplastic ROS induced cell death. Through the genetic analysis we identified WRKY70 and SGT1b as cell death regulators functioning downstream of RCD1 and show that quantitative rather than qualitative differences in gene expression related to cell death appeared to better explain the outcome. Allocation of plant energy to defenses diverts resources from growth. Recently, a plant response termed stress-induced morphogenic response (SIMR) was proposed to regulate the balance between defense and growth. Using a rcd1 double mutant collection we show that SIMR is mostly independent of the classical plant defense signaling pathways and that the redox balance is involved in development of SIMR.
植物对环境条件变化的响应是由一系列信号转导事件介导的，这些事件会导致下游响应，包括基因表达的变化和细胞死亡程序的激活。拟南芥的自由基诱导细胞死亡1（RCD1）被认为通过与转录因子的蛋白质-蛋白质相互作用来调节植物的应激反应。此外，rcd1突变体在响应质外体活性氧（ROS）时对细胞死亡的控制存在缺陷。我们结合转录组学和功能基因组学方法，首先在时间序列中使用微阵列分析来研究rcd1质外体ROS处理后基因表达的变化。为了确定一组核心的细胞死亡调控基因，将RCD1调控的基因与来自经历细胞死亡或用各种病原体、植物激素或其他化学物质处理的植物的其他阵列实验聚类在一起。随后，构建了选定的rcd1双突变体，以进一步确定质外体ROS诱导细胞死亡执行的遗传需求。通过遗传分析，我们确定WRKY70和SGT1b作为在RCD1下游起作用的细胞死亡调节因子，并表明与细胞死亡相关的基因表达的定量而非定性差异似乎更好地解释了结果。植物将能量分配到防御中会使资源从生长中转移。最近，一种被称为应激诱导形态发生反应（SIMR）的植物反应被提出用于调节防御和生长之间的平衡。使用rcd1双突变体集合，我们表明SIMR大多独立于经典的植物防御信号通路，并且氧化还原平衡参与了SIMR的发展。
