Plant immune signaling network: Connecting pathogen perception, chromatin modification and activation of immune responses.

植物病原体是农作物生产面临的挑战。特别是，真菌病原体引起破坏性疾病，威胁全球粮食、饲料和纤维生产，危害植物物种多样性。扩大植物如何抵御微生物感染的基础知识的研究有望帮助设计更好的疾病控制策略。多方面的分子，生物化学和基因组的方法将被部署，以了解植物如何调节激活防御病原体。植物激活一系列防御机制，包括合成各种抗菌剂和其他免疫反应，以阻止感染或限制感染后的损害程度。植物如何激活或抑制这些机制将被研究。了解这些变化的时空调控对于了解抗病机制具有重要意义。在没有病原体的情况下，这些免疫反应中的一些过早激活对植物是不利的。因此，严格控制时间和空间激活是至关重要的。这种防御基因激活，重编程，以及如何发生在真核DNA的背景下，是挤满了染色质的分子和生化机制将被确定。将分析将病原体感测与植物细胞中的防御激活联系起来的细胞通信。该项目的发现将扩大基础知识，并为开发抗病植物铺平道路。培养植物分子生物学专业本科生、研究生和博士后。植物免疫基因的转录是植物免疫的重要组成部分，在对病原体的应答中发生快速和大量的转录编程。组蛋白修饰酶（HME）介导的组蛋白修饰平衡的变化是协调这些细胞反应的关键因素。然而，在染色质的情况下，转录重编程响应感染的机制还不清楚。本计画将剖析病原体感应与组蛋白修饰之间的讯号传递路径，以及染色质可及性与转录的动态变化。将使用具有拮抗性生化和功能的组蛋白甲基转移酶和去甲基酶研究组蛋白赖氨酸甲基化（HLM）平衡偏移的调节影响。可逆组蛋白修饰和随后的基因表达变化之前的分子机制和调控因素将被阐明。将研究调节HME活化和募集至靶基因座以响应感染以触发HLM和免疫基因转录的转变的因素。转录因子和核小体组装蛋白的功能伙伴的HME基因调控将进行分析。Aim1专注于通过蛋白激酶调节HME，将免疫反应中的早期事件与染色质状态和基因表达的变化联系起来。目的2是研究HME相互作用转录因子和核小体组装蛋白的功能。目的3是确定HLM平衡变化的基因组范围内的基因表达谱，并破译其生物学影响。该项目的发现将改善基础知识，并为性状的表观基因组修饰铺平道路。最后，该项目将培养本科生、研究生和博士后科学家。该奖项反映了NSF的法定使命，并通过使用基金会的知识价值和更广泛的影响审查标准进行评估，被认为值得支持。

Plant pathogens are challenges to crop production. In particular, fungal pathogens cause destructive diseases that threaten global food, feed and fiber production and jeopardize diversity of plant species. Studies that expand fundamental knowledge on how plants fend off microbial infection is expected to help design better disease control strategies. Multifaceted molecular, biochemical and genomic approaches will be deployed to understand how plants regulation activation of defense against pathogens. Plants activate a battery of defense mechanisms including the synthesis of diverse antimicrobial agents and other immune responses to deter infection or restrict the extent of damage after infection. How plants activate or suppress these mechanisms will be studied. Knowledge on the temporal and spatial regulation of such changes are important to understand the mechanisms of disease resistance. The untimely activation of some of these immune responses in the absence of pathogens is not beneficial to the plant. Consequently a tight control of on timing and spatial activation is critical. The molecular and biochemical mechanisms underlying such defense gene activation, reprogramming, and how these occurs in the context of eukaryotic DNA that is packed with chromatin will be determined. The cellular communication that link pathogen sensing to the activation of defense in the plant cell will be analyzed. Discoveries from this project will expand basic knowledge, and pave the way to develop disease resistant plants. Finally, this project will train undergraduate, graduate students and post-doctoral scientists in plant molecular biology. Plant immune gene transcription is a major component of plant immunity with rapid and massive transcriptional programming occurring in response to pathogens. Changes in equilibrium of histone modifications mediated by histone modifying enzymes (HMEs) are critical players orchestrating these cellular responses. However, the mechanisms underlying transcription reprogramming in response to infection in the context of chromatin are not understood. This project is to dissect the signal transduction pathway connecting pathogen sensing to histone modifications, and the consequent dynamics in chromatin accessibility and transcription. The regulatory impacts of shifts in equilibrium of histone lysine methylations (HLMs) will be studied using histone methyl transferases and demethylases with antagonistic biochemical and functions. Molecular mechanisms and factors regulating events preceding reversible histone modifications and the subsequent changes in gene expression will be elucidated. Factors that regulate activation and recruitment of HMEs to target loci in response to infection to trigger shifts in HLMs and immune gene transcription will be studied. Transcription factors and nucleosome assembly proteins that are functional partners of HMEs in gene regulation will be analyzed. Aim1 focuses on regulation of HMEs by protein kinases, linking early events in immune responses to changes in chromatin state and gene expression. Aim2 is to characterize the functions of HME interacting transcription factors (TFs) and nucleosome assembly proteins. Aim3 is to determine genome wide gene expression profiles underlying shifts in equilibrium of HLM and decipher its biological impact. Discoveries from this project will improve basic knowledge and pave the way for epi-genome modifications of traits. Finally, this project will train undergraduate, graduate students and post-doctoral scientists.This award reflects NSF's statutory mission and has been deemed worthy of support through evaluation using the Foundation's intellectual merit and broader impacts review criteria.