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Study of chloroplast stromules during PCD and inter-organellar communication

PCD 和细胞间通讯过程中叶绿体基质的研究

基本信息

批准号：
9382027
负责人：
Jeffrey L Caplan
金额：
$ 32.22万
依托单位：
UNIVERSITY OF CALIFORNIA AT DAVIS
依托单位国家：
美国
项目类别：
财政年份：
2011
资助国家：
美国
起止时间：
2011-07-15 至 2019-05-19
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/9382027
关键词：
Actins Animals Apoptosis Binding Biological Models Carrier Proteins Cell Death Cell Nucleus Cell Survival Cell membrane Cell surface Cellular biology Chloroplasts Communicable Diseases Communication Complex Computing Methodologies Cytoplasm Cytoskeleton Development Disease Flagellin Generations Genetic Goals Growth and Development function Hormones Hydrogen Peroxide Hypersensitivity Immune Immune response Immune signaling Immunity Immunologic Receptors Infection Innate Immune Response Knock-out Leucine-Rich Repeat MAP Kinase Gene Malignant Neoplasms Mammals Mass Spectrum Analysis Measures Membrane Microfilaments Microtubules Mitochondria Modeling Molecular Morphology Movement NADPH Oxidase Natural Immunity Nuclear Nucleotides Organelles Pattern Pattern recognition receptor Phosphotransferases Plants Play Process Proteins Proteomics Publishing RIPK1 gene Reactive Oxygen Species Recruitment Activity Regulation Research Role Salicylic Acids Signal Transduction Signaling Protein Source Testing Tubular formation Vertebrates Virulence base extracellular genetic analysis genetic approach immune function insight mutant novel optogenetics organelle movement pathogen prevent protein biomarkers protein transport receptor response superoxide-generating NADPH oxidase tool

项目摘要

Project Summary This project focuses on chloroplasts as central player in the generation of immune signals and the regulation of programmed cell death (PCD) required for innate immune responses against pathogen infection. Although mitochondria play a central role during mammalian PCD, emerging evidence suggests that in plants chloroplasts have a critical function in executing localized PCD that limits pathogen spread. Chloroplasts in addition to being involved in the generation of immune signals such as reactive oxygen species (ROS) and defense hormone salicylic acid (SA), also participate directly in the recognition of pathogen. Interestingly, the chloroplasts dynamically change their morphology during immune responses and send out tubular projections called stromules. These induced stromules use the cytoskeleton to extend and then anchor to the nucleus, which facilitate perinuclear clustering of chloroplasts and transport chloroplast-generated ROS and defense proteins to the nucleus. The overall goal of this application is to use combination of novel cell biology, genetics, proteomics and computational approaches to unravel the mechanistic basis of stromule driven periunclear chloroplast clustering and determine the identity and function of immune signals released from chloroplasts to nuclei. Specifically, Aim 1 will examine organelle and cytoskeleton dynamics during plant innate immunity. Novel computational methods quantifying stromule features and dynamics will be further developed and applied to understand chloroplasts, their stromules, and cytoskeleton dynamics during innate immunity. Both plant and animal pathogens target the cytoskeleton, and this aim will examine how pathogen effectors alter the cytoskeleton and related organelle dynamics as a virulence strategy. Aim 2 will investigate immune signals required for stromule induction and the release of chloroplast signals. The relationship of different ROS sources, organelle movement and PCD during immune responses will be examined using a combination of genetic tools and the computational methods developed in Aim 1. In Aim 3, known chloroplast-derived immune signals will be characterized and novel protein signals will be identified. The downstream targets of H2O2 in the nucleus will be elucidated and studied. Mass spectrometry will be used to identify proteins that are transported from chloroplasts to nuclei. Genetic approaches will be employed to examine their role during PCD. Lastly, the mechanism of release from chloroplasts during innate immunity will be studied to determine if it is akin to mitochondrial release during apoptosis in mammals. Understanding the role of different organelles during PCD and innate immunity will provide a unified mechanistic basis of cell death and cell survival process that occur in response to infectious pathogens. The results from our model systems will impact broadly on understanding of organelle-to-nuclear communication that influence innate immunity against infectious diseases.

项目总结