背景回顾：Signaling events triggered by hydrogen peroxide (H2O2) regulate plant growth and defense by orchestrating a genome-wide transcriptional reprogramming. 

提出问题：However, the specific mechanisms that govern H2O2-dependent gene expression are still poorly understood. 

主要发现：Here we identify the Arabidopsis Mediator complex subunit MED8 as a regulator of H2O2 responses. 

结果1-med8突变：The introduction of the med8 mutation in a constitutive oxidative stress genetic background (catalase-deficient, cat2) was associated with enhanced activation of the salicylic acid pathway and accelerated cell death. 

结果2-med8突变与SA、JA：Interestingly, med8 seedlings were more tolerant to oxidative stress generated by the herbicide methyl viologen and exhibited transcriptional hyperactivation of defense signaling, in particular salicylic acid- and jasmonic acid-related pathways. The med8-triggered tolerance to methyl viologen was manipulated by introduction of secondary mutations in salicylic acid and jasmonic acid pathways. 

结果3-MED8互作：In addition, analysis of the Mediator interactome revealed interactions with components involved in mRNA processing and microRNA biogenesis, hence expanding the role of Mediator beyond transcription. Notably, MED8 interacted with the transcriptional regulator NEGATIVE ON TATA-LESS, NOT2, to control the expression of H2O2-inducible genes and stress responses. 

结论：Our work establishes MED8 as a component regulating oxidative stress responses and demonstrates that it acts as a negative regulator of H2O2-driven activation of defense gene expression

 摘 要 

由过氧化氢（H2O2）诱导的信号事件通过全基因组范围的转录重编程调控植物生长和防御。但是，赋予H2O2依赖型的基因表达的分子机制还不清楚。本文中，作者发现拟南芥转录中介复合物亚基MED8作为H2O2响应的调控子发挥功能。在组成型氧化应激遗传背景下（即过氧化氢酶突变体cat2），引入med8突变，会表现出水杨酸途径的激活增强和细胞死亡加速等表型。有趣的是，med8突变体幼苗对由除草剂甲基紫精处理产生的氧化应激更具耐受性，而且防御信号转导存在转录超激活，尤其是水杨酸和茉莉酸相关的途径。通过向med8突变体引入另外的水杨酸和茉莉酸通路上的突变，会影响med8突变体对于除草剂甲基紫精的耐受性。另外，对于转录中介体的互作组分析显示其与mRNA加工和microRNA生物发生相关组分之间存在互作，从而将转录中介体的功能扩展到了转录之外。尤其是，MED8会与转录调控子NOT2互作，从而控制受H2O2诱导的基因的表达和胁迫响应。本文的工作揭示了MED8作为调控氧化应激反应的组分发挥作用，并证明其是H2O2驱动的防御基因表达激活的负调节因子。