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Investigating How Chromatin Remodeling Affects Endocytosis and Synapse Organization

Investigating How Chromatin Remodeling Affects Endocytosis and Synapse Organization
研究染色质重塑如何影响内吞作用和突触组织
批准号:
10121448
负责人:
FAITH L LIEBL
金额:
$6.87万
依托单位国家:
美国
项目类别:
财政年份:
2020
资助国家:
美国
项目状态:
已结题
起止时间:
2020-07-01 至 2022-06-30
关键词:
Adaptor Signaling ProteinAdultAffectAlzheimer&aposs DiseaseAlzheimer&aposs disease pathologyAmyloid beta-ProteinAmyloid beta-Protein PrecursorAnimalsAppearanceBindingBiologyBrain DiseasesC-terminalCHARGE syndromeCHD7 geneCell Adhesion MoleculesCessation of lifeChromatinCleaved cellComplementComplexDNA-Binding ProteinsDataDrosophila genusDrosophila inturned proteinDrosophila melanogasterEndocytosisEnzymesEpigenetic ProcessExhibitsFunctional disorderGenesGenetic TranscriptionGenomeGlutamate ReceptorGoalsHTATIP geneHippocampus (Brain)HistonesHomologous ProteinHumanHuman Amyloid Precursor ProteinImpaired cognitionImpairmentInstitutionIntegral Membrane ProteinIntestinesLeadLocomotionMemory impairmentMolecularMusMutationNerve DegenerationNeuraxisNeurodevelopmental DisorderNeuromuscular JunctionNeuronsOrthologous GenePathologyPeptidesPhenocopyPhysiologicalPlayProcessProtein Binding DomainProtein FragmentProteinsRecyclingResearchRoleSenile PlaquesSignal TransductionStudentsSynapsesSynaptic TransmissionSynaptic VesiclesTestingTranscriptTranscription Initiation SiteWorkamyloid precursor protein processingautism spectrum disorderbasebeta-site APP cleaving enzyme 1bonebrain cellchromatin remodelingdifferential expressionexperimental studyflygamma secretasehelicaseimprovedinsightloss of functionloss of function mutationmolecular pathologymutantneurofibrillary tangle formationneurotoxicneurotransmissionoverexpressionparent grantpostsynapticpresynapticprotein expressionprotein functionrecruitsecretasestem cellssynaptic functionundergraduate student

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Project Summary The transmembrane protein β-amyloid precursor protein (APP) is central to the pathophysiology of Alzheimer’s disease (AD). The β-amyloid hypothesis posits that aberrant processing of APP leads to the formation of β- amyloid aggregates, which are neurotoxic leading to the cognitive impairments observed in AD. Despite the importance of APP in AD, little is known about its function or how neurons regulate its expression. We have found that Kismet (Kis), a chromatin remodeling protein in Drosophila, regulates expression of APP-like and neuronal processes that are dysregulated in AD. Kis is similar to the mammalian chromatin helicase binding domain (CHD) proteins CHD7 and CHD8, both of which are implicated in neurodevelopmental disorders including CHARGE Syndrome and autism spectrum disorders, respectively, and synaptic function. The goal of this proposal is to better understand how the epigenetic chromatin remodeling protein, Kis, regulates APP-like expression in animals. Mutations in kis lead to increased levels of APP-like in neurons and of cell adhesion molecules at the synapse. The latter are known to interact with APP and APP-like. We hypothesize that Kis promotes synaptic function and organization by suppressing synaptic levels of APP-like thereby affecting the recycling of synaptic vesicles. To test this hypothesis, we will first better characterize the functional interaction between Kis and APP-like. Then we will determine whether Kis and APP-like work cooperatively to influence synaptic vesicle endocytosis and localize cell adhesion molecules to the synapse. These data will help us better understand how chromatin remodeling proteins enable synapse function and provide mechanistic insight into the pathology of AD.
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