Characterization of lipid signaling altered by T3S effector AvrBsT

T3S 效应子 AvrBsT 改变脂质信号传导的表征

基本信息

批准号：
8268412
负责人：
Mary Beth MUDGETT
金额：
$ 32.31万
依托单位：
STANFORD UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2004
资助国家：
美国
起止时间：
2004-09-30 至 2014-04-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8268412
关键词：
Animals Apolipoproteins Arabidopsis Bacteria Bacterial Infections Binding Binding Proteins Biochemical Biological Models Cell membrane Cells Eukaryota Event Family Funding Genes Genetic Genetic Models Genetic Screening Goals Homeostasis Immune response Immune system Immunity Infection Knowledge Lipase Lipid Binding Lipids Mediating Metabolic Pathway Natural Immunity Outcome Phenotype Phosphatidic Acid Phospholipase D Phospholipid Metabolism Phospholipids Physiology Plant Diseases Plant Physiology Plant Proteins Plants Prevention Proteins Resistance Role Second Messenger Systems Signal Transduction Substrate Specificity System Tissues Work bacterial resistance biochemical model defense response insight lipid metabolism member mutant novel overexpression pathogen pathogenic bacteria protein function public health relevance response second messenger

项目摘要

DESCRIPTION (provided by applicant): 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. Comprehensive 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. PUBLIC HEALTH RELEVANCE: 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.

描述（由申请人提供）：植物和动物的细菌病原体使用 III 型分泌（T3S）系统和效应蛋白底物来改变真核生理学，以促进细菌繁殖和宿主定植。植物病原细菌中大量的 T3S 效应子（约 20-30 种蛋白质）预测植物信号级联中的多个节点将成为目标。然而，人们对植物靶标的身份以及这些 T3S 效应蛋白操纵植物生理学的生化机制知之甚少。广泛的表型研究支持许多 T3S 效应子抑制植物免疫系统在组织中定殖的概念。这阐明了基础防御反应和抗性（R）蛋白介导的先天免疫反应在控制植物界细菌感染结果中的重要性。了解植物免疫如何调节以及细菌病原体如何操纵宿主是预防和消除植物病害所需的基础知识。该项目的长期目标是阐明植物如何整合脂质信号来应对细菌感染。两种保守的真核蛋白——SOBER1（一种脂肪酶）和 CIP（一种推定的载脂蛋白）——已被鉴定并被证明是植物先天免疫反应的重要调节因子。将使用拟南芥病理系统进行全面的遗传和生化研究，以表征 SOBER1 和 CIP 底物特异性，并确定这些蛋白质在细菌感染期间控制磷脂代谢和信号传导的机制。研究还将旨在确定病原体 T3S 效应子 AvrBsT 扰乱受感染植物细胞内脂质稳态的生化机制。这项工作有望为植物控制脂质代谢和响应病原体攻击的信号转导的生化机制提供基础见解。越来越多的证据表明植物和动物的脂质代谢和免疫之间存在相互作用，这表明有关脂质信号如何启动和终止的基础知识对于充分了解真核生物中免疫系统的调节至关重要。公共卫生相关性：了解植物免疫如何调节以及细菌病原体如何操纵宿主是预防和消除植物病害所需的基础知识。