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Stress-induced phenotypic plasticity in C. elegans

线虫中应激诱导的表型可塑性

基本信息

批准号：
9335927
负责人：
Nathan Schroeder
金额：
$ 28.93万
依托单位：
UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN
依托单位国家：
美国
项目类别：
财政年份：
2014
资助国家：
美国
起止时间：
2014-09-15 至 2019-08-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/9335927
关键词：
Ablation Adult Affect Afferent Neurons Anatomy Animal Model Animals Axon Behavioral Bioinformatics Biological Models Brain Caenorhabditis elegans Chronic Cilia Cleaved cell Collaborations Complex Data Defect Dendrites Development Environment Evolution Food Genes Genetic Genetic Epistasis Goals Grant Health Hibernation Homologous Gene Human IL2 gene Investigation Lasers Length Letters Modeling Molecular Morphology Muscle Cells Mutagenesis Nervous system structure Neuronal Plasticity Neurons Orthologous Gene Output Pathology Pathway interactions Pattern Phenotype Plasticizers Positioning Attribute Post-Traumatic Stress Disorders Postdoctoral Fellow Property Proprotein Convertases Reagent Research Personnel Resistance Role Signal Transduction Stimulus Stress Testing Transmission Electron Microscopy Vascular Smooth Muscle behavioral plasticity coping developmental plasticity driving force experimental study forward genetics genetic approach intercellular communication mutant novel public health relevance response stress related disorder targeted treatment

项目摘要

DESCRIPTION (provided by applicant): Environmental stress has direct but complex effects on human health. Phenotypic plasticity in response to environmental stress may result in both adaptations necessary for survival as well as pathologies detrimental to well-being. The model organism Caenorhabditis elegans enters into a stress-resistant 'dauer' stage in response to adverse environmental conditions. The dauer is a classic example of developmental and behavioral plasticity. We previously showed that the dauers undergo extensive and reversible neuronal remodeling in a set of IL2 sensory neurons and that this remodeling is dependent on the furin homolog, KPC-1. During this grant period we will: 1) Extend our investigations into the role of KPC-1 in remodeling by identifying substrates. Furthermore, we will investigate the role of KPC-1 in additional stages of phenotype plasticity in C. elegans. 2) Characterize mutants isolated from a mutagenesis screen that are defective in IL2 remodeling 3) Analyze the ultra-structural properties of the IL2 to uncover the requirements necessary for their inherent plasticity.

描述(申请人提供)：环境压力对人类健康有直接但复杂的影响。对环境压力的表型可塑性可能导致生存所必需的适应，也可能导致损害福祉的病理。在恶劣的环境条件下，模式生物秀丽线虫进入了抗逆性‘达尔’阶段。达尔是发育和行为可塑性的典型例子。我们以前证明了Dauer在一组IL2感觉神经元中经历了广泛和可逆的神经元重塑，并且这种重塑依赖于Furin同系物KPC-1。在此授权期内，我们将：1)通过识别底物来扩展我们对KPC-1在重塑中的作用的研究。此外，我们将研究KPC-1在线虫表型可塑性的其他阶段中的作用。2)鉴定从突变筛选中分离出的在IL2重塑方面存在缺陷的突变体。3)分析IL2的超微结构属性，以揭示其固有可塑性所必需的要求。