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:8927662
- 负责人:
- 金额:$ 26万
- 依托单位:
- 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:
- 关键词:AblationAccountingAdultAffectAfferent NeuronsAnimal ModelAnimalsAxonBehavioralBioinformaticsBiological ModelsBlood VesselsBrainCaenorhabditis elegansChronicCiliaCleaved cellCollaborationsComplexDataDefectDendritesDevelopmentEnvironmentEvolutionFoodGenesGeneticGenetic EpistasisGoalsGrantHealthHibernationHomologous GeneHumanIL2 geneInvestigationLasersLengthLettersModelingMolecularMorphologyMutagenesisNervous system structureNeuronal PlasticityNeuronsOrthologous GeneOutputPathologyPathway interactionsPatternPersonal SatisfactionPhenotypePlasticsPositioning AttributePost-Traumatic Stress DisordersPostdoctoral FellowPropertyProprotein ConvertasesReagentResearch PersonnelResistanceRoleSignal TransductionSmooth Muscle MyocytesStagingStimulusStressTestingTransmission Electron Microscopycopingdevelopmental plasticitydriving forceforward geneticsintercellular communicationmutantnovelresearch studyresponsestress related disordertargeted 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。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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Nathan Schroeder其他文献
Nathan Schroeder的其他文献
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{{ truncateString('Nathan Schroeder', 18)}}的其他基金
Stress-induced phenotypic plasticity in C. elegans
线虫中应激诱导的表型可塑性
- 批准号:
8749979 - 财政年份:2014
- 资助金额:
$ 26万 - 项目类别:
Stress-induced phenotypic plasticity in C. elegans
线虫中应激诱导的表型可塑性
- 批准号:
9128668 - 财政年份:2014
- 资助金额:
$ 26万 - 项目类别:
Stress-induced phenotypic plasticity in C. elegans
线虫中应激诱导的表型可塑性
- 批准号:
9335927 - 财政年份:2014
- 资助金额:
$ 26万 - 项目类别:
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