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Understanding the effects of mitochondrial fission disruption during early cortical development
Organization VANDERBILT UNIVERSITYLocation Nashville, UNITED STATESPosted 5 Dec 2022Deadline 31 Dec 2024 ⚠️
NIHUS FederalResearch GrantFY20250-11 years oldActinsAddressAdoptedAffectApoptosisApoptosis PathwayBindingBrainBrain Nervous SystemCalciumCell BodyCell LineCell modelCellLineCellsCellular modelChildChild YouthChildren (0-21)ComplexDNA mutationDefectDephosphinDevelopmentDevelopmental DelayDevelopmental Delay DisordersDynaminDysfunctionEncephalonEndoplasmic ReticulumEpilepsyEpileptic SeizuresEpilepticsErgastoplasmEventExhibitsF-ActinFeedbackFibroblastsFilamentous ActinFunctional disorderGTPGTP PhosphohydrolasesGTPasesGenetic ChangeGenetic defectGenetic mutationGuanosine TriphosphateGuanosine Triphosphate PhosphohydrolasesGuanosinetriphosphatasesHeterozygoteHumanHydrolysisImmune PrecipitationImmunoprecipitationImpairmentInvestigationKnowledgeLeadMembraneMetabolicMicrocephalyMicroscopyMitochondriaMitochondrial DiseasesMitochondrial DisordersModelingModern ManMolecularMolecular InteractionMorphologyMotilityMutationNatureNerve CellsNerve UnitNeural CellNeural DevelopmentNeural Stem CellNeuritesNeurocyteNeurodevelopmental DeficitNeurodevelopmental DisorderNeurological Development DisorderNeuronal DifferentiationNeuronsOptic AtrophyOrganellesOutcomePathogenicityPathologicPathologyPatientsPb elementPhenotypePhysiopathologyProcessProgenitor CellsProgrammed Cell DeathProteinsReceptor ProteinResolutionRoleSeizure DisorderSeizuresSiteSpecific Child Development DisordersStrains Cell LinesSymptomsSynapsesSynapticTIRF MicroscopyTestingTotal Internal Reflection FluorescentTotal Internal Reflection Fluorescent Microscopyaxon growthaxonal growthcell typeconstrictioncultured cell linede novo mutationde novo variantdevelopmentalearly childhoodepilepsiaepileptic encephalopathiesepileptogenicexome sequencingexome-seqgenome mutationguanosinetriphosphataseheavy metal Pbheavy metal leadheterozygosityiPSiPSCiPSCsimprovedindividualized therapeuticinduced pluripotent cellinduced pluripotent stem cellinduced pluripotent stem cells derived from patientsinduced pluripotent stem cells from patientsinducible pluripotent cellinducible pluripotent stem cellinsightkidsloss of function mutationmembrane structuremicrencephalymicroencephalymitochondria fitnessmitochondrialmitochondrial based therapeuticsmitochondrial fitnessmitochondrial membranemitochondrial targeted therapeuticsmitochondrial therapeuticsmitotherapeuticsmutantnerve stem cellneural precursorneural precursor cellneural progenitorneural progenitor cellsneural stem and progenitor cellsneurodevelopmentneurodevelopmental diseaseneurogenesisneurogenic progenitorsneurogenic stem cellneuron developmentneuron progenitorsneuronalneuronal developmentneuronal progenitorneuronal progenitor cellsneuronal stem cellsneuroprogenitornovelpathophysiologypatient derived human iPSpatient derived human iPSCpatient derived human induced pluripotent stem cellpatient derived iPSpatient derived iPSCpatient derived induced pluripotent cellspatient derived induced pluripotent stem cellspatient variabilitypatient variationpatient-derived pluripotent stem cellspersonalized therapeuticprogenitor and neural stem cellsprogenitor cell fateprogenitor fatereceptorresolutionssocial rolestem and progenitor cell fatestem cell fatestem cellssuper high resolutionsuperresolutionsynapsesynapse formationsynaptogenesistraffickingultra high resolutionvariability between patientsvariation between patientsyoungster
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Description preview
Summary
With the advent of exome sequencing, a growing number of children are being identified with de novo loss of
function mutations in the large GTPase essential for mitochondrial fission - Dynamin Related Protein 1 (DRP1);
these mutations result in severe neurodevelopmental phenotypes such as developmental delay, optic atrophy,
and epileptic…
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