Dissection of AvrBsT-BST defense pathway in Arabidopsis

植物和动物的细菌病原体使用III型分泌（T3 S）系统， 效应蛋白底物改变真核生物生理学以促进细菌 繁殖和宿主定殖。T3 S效应子的大库（~20-30 植物病原菌中的蛋白质）预测植物信号传导中的多个节点 级联成为目标。植物目标的身份和生物化学 然而，这些T3 S效应蛋白操纵植物生理学的机制 我们对此知之甚少。广泛的表型研究支持这一概念，许多 T3 S效应子抑制植物免疫系统在组织中定殖。这 阐明了基础防御反应和抗性（R）蛋白的重要性- 介导的先天性免疫反应在控制细菌感染的结果， 植物王国了解植物免疫力是如何调节的，以及细菌如何 病原体操纵其宿主是预防所需的基本知识 和消除植物病害。 该项目的长期目标是阐明植物如何整合脂质信号， 对细菌感染有反应。两个保守的真核生物蛋白--脂肪酶SOBER 1 和CIP，一种假定的载脂蛋白-已被确定并显示出重要性 植物先天免疫反应的调节因子。遗传和生物化学研究将 使用拟南芥病理系统来表征SOBER 1和CIP 底物特异性，并确定这些蛋白质控制的机制 磷脂代谢和信号转导。研究还将 目的是确定病原体T3 S效应子 AvrBsT干扰受感染植物细胞内的脂质稳态。这项工作预计将 提供基本的见解，以生物化学机制所使用的植物控制 脂质代谢和信号传导对病原体攻击的响应。了越来越多的 有证据表明两种植物的脂质代谢和免疫力之间存在相互作用， 动物实验表明，关于脂质信号如何启动的基础知识 对于完全理解免疫系统是如何调节的至关重要 在真核生物中。

Bacterial pathogens of plant and animals use the type III secretion (T3S) system and effector protein substrates to alter eukaryotic physiology to promote bacterial multiplication and host colonization. The large repertoire of T3S effectors (~20-30 proteins) in plant pathogenic bacteria predicts that multiple nodes in plant signaling cascades are being targeted. The identity of the plant targets and the biochemical mechanisms by which these T3S effector proteins manipulate plant physiology however are poorly understood. Extensive phenotypic studies support the concept that many of the T3S effectors suppress the plant immune system to colonize tissues. This illuminates the importance of basal defense responses and resistance (R) protein- mediated innate immune responses in controlling the outcome of bacterial infections in the plant kingdom. Understanding how plant immunity is regulated and how bacterial pathogens manipulate their hosts is fundamental knowledge required for the prevention and elimination of plant disease. The long-term goal of this project is elucidate how plants integrate lipid signals to respond to bacterial infection. Two conserved eukaryotic proteins - SOBER1, a lipase and CIP, a putative apolipoprotein - have been identified and shown to be important regulators of innate immune responses in plants. Genetic and biochemical studies will be performed using the Arabidopsis pathosystem to characterize SOBER1 and CIP substrate specificity and to determine the mechanisms by which these proteins control phospholipid metabolism and signaling during bacterial infection. Studies will also be aimed to determine the biochemical mechanisms by which the pathogen T3S effector AvrBsT perturbs lipid homeostasis within infected plant cells. This work is expected to provide fundamental insight to the biochemical mechanisms used by plants to control lipid metabolism and signaling in response to pathogen attack. The growing body of evidence suggesting an interplay between lipid metabolism and immunity in both plants and animals indicates that fundamental knowledge about how lipid signals are initiated and terminated will be essential to fully understand how the immune system is regulated in eukaryotes.