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The Perception of Mitochondrial Stress in Receiving Cells

接收细胞中线粒体应激的感知

基本信息

批准号：
9052328
负责人：
Andrew G Dillin
金额：
$ 40.95万
依托单位：
UNIVERSITY OF CALIFORNIA BERKELEY
依托单位国家：
美国
项目类别：
财政年份：
2016
资助国家：
美国
起止时间：
2016-06-01 至 2021-03-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/9052328
关键词：
Address Affect Age of Onset Aging Aging-Related Process Animals Biogenesis Caenorhabditis elegans Cells Communication Complex Cytosol Disease Distal Double-Stranded RNA Electron Transport Environment Eukaryotic Cell Event Exposure to Gene Expression Genetic Genetic Epistasis Homeostasis Intestines Longevity Mitochondria Mitochondrial DNA Modification Morphology Mutation Nematoda Nervous system structure Neurodegenerative Disorders Neurological observations Neurons Organ Organism Oxidation-Reduction Pathway interactions Perception Peripheral Play Ploidies Population Predisposition Production Property Receptor Signaling Respiration Role Signal Pathway Signal Transduction Sorting - Cell Movement Stress System Techniques Tissues Toxic Environmental Substances Translations Up-Regulation Variant Whole Organism biological adaptation to stress cell type complex IV environmental change extracellular fitness genome-wide analysis innovation knock-down mitochondrial dysfunction programs promoter protein folding response sensor

项目摘要

It was recently discovered that reduced ETC signaling in neuronal cells is sufficient to extend the lifespan of C. elegans. It was also found that this effect is dependent upon the activity of an essential component of the mitochondrial stress response or UPRmt. It is not yet understood, however, the fundamental mechanisms by which this life span extension occurs or how the signal is sent and perceived. Moreover, the essential role that the mitochondrion has in cellular homeostasis and energy production suggests that it may act as a reactive sensor of random intrinsic or extrinsic variables capable of influencing an organism's susceptibility to disease. Changes within the mitochondria thus also might be responsible for the emergent properties displayed in such a system in response to stochastic changes, and/or may play a significant role in coordinating the activation of non-mitochondrial stress response pathways. A prediction that genetic modifications will decrease the capacity for stochastic variation in mitochondrial function will ultimately negatively affect the fitness of the organism. Such a hypothesis is in keeping with recent evidence suggesting that deleterious mutations actually decrease the sensitivity of gene expression in response to small environmental changes (a loss of phenotypic robustness). A further hypothesis is it may predict co-variance between the UPRmt and stress response pathways, currently thought to act in distinct regulatory networks, and seek to discover the potential mechanisms by which this co-variance occurs.

最近发现，神经细胞ETC信号的减少足以延长C的寿命。