Decoding neural cell fate diversity
解码神经细胞命运多样性
基本信息
- 批准号:10283597
- 负责人:
- 金额:$ 40.56万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2021
- 资助国家:美国
- 起止时间:2021-09-01 至 2024-02-29
- 项目状态:已结题
- 来源:
- 关键词:AddressAdoptedArchitectureAxonBehaviorBioinformaticsBrainCRISPR screenCandidate Disease GeneCell SeparationCell SurvivalCellsCessation of lifeDaughterDevelopmentDevelopmental ProcessDiseaseElementsEmbryoEventFluorescenceFoundationsGene Expression ProfileGene Expression ProfilingGenesGeneticIn Situ HybridizationIndividualInjuryIon ChannelKnowledgeLearningLifeModelingMolecularMotor NeuronsMuscleMuscle FibersNervous System PhysiologyNervous system structureNeuronsOpticsPathway interactionsPopulationProcessProtocols documentationRNAResearchRoleSignal PathwaySpinalSurveysSynapsesSystemTarget PopulationsTechniquesTestingTimeTranscriptTransgenic OrganismsVertebratesZebrafishdifferential expressionexperimental studygene discoveryinnovationinsightmolecular markernerve stem cellnerve supplyneurodevelopmentneuron developmentneuron losssingle-cell RNA sequencingtherapeutic targettooltranscription factor
项目摘要
PROJECT SUMMARY/ABSTRACT
Cell fate diversification is a critical step in producing the many neuronal subtypes required for
functional circuitry in the vertebrate brain. We know a considerable amount about how neural
progenitors diversify fates to form distinct daughter neurons. However, much less is known
about later processes that diversity the fates of postmitotic neurons. One reason for this
knowledge gap is that in most vertebrate models it is impossible to recognize and study
precisely the same neurons in separate individuals, limiting predictive and statistical power. We
can overcome these limitations in zebrafish by studying two adjacent, individually identifiable,
spinal motoneurons. We discovered that these neurons are initially equivalent, and that
interactions between them, in addition to interactions with an identified set of muscle fibers,
breaks the equivalence between the two neurons and causes them to adopt distinct fates.
Moreover, one of these neurons then typically dies, an important fate for sculpting brain
architecture and circuitry. This is a unique situation in vertebrates, in which we can observe fate
diversification as it is occurring in living embryos and predict that a neuron will die well before
the process occurs, yet we still do not know the underlying molecular events. We will overcome
this barrier using a variety of tools that enable us to manipulate the fates of these two neurons
and single cell RNA sequencing at defined stages during the developmental process. This
combination with enable us to discover genes involved in neuronal cell fate diversification as
well as genes that predict neuronal cell death and survival. We plan to validate these genes
using quantitative RNA in situ hybridization techniques. We will then test validated candidates
using an innovative F0 CRISPR screen. Our proposed studies will reveal genes previously
unknown to function during neuronal cell fate diversification, survival, and death. If successful,
they will uncover genetic mechanisms of neuronal cell fate diversification with unprecedented
precision, and thus will open new avenues of inquiry and deepen our understanding of
neurodevelopmental mechanisms.
项目总结/文摘
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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JUDITH S EISEN其他文献
JUDITH S EISEN的其他文献
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Identification of bacterial products required for brain development
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- 批准号:
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- 资助金额:
$ 40.56万 - 项目类别:
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NICHD R25 Summer Research Program at the University of Oregon
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8217333 - 财政年份:2011
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俄勒冈大学 NICHD R25 夏季研究项目
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8298973 - 财政年份:2011
- 资助金额:
$ 40.56万 - 项目类别:
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8660316 - 财政年份:2011
- 资助金额:
$ 40.56万 - 项目类别:
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