2019
Id4 Downstream of Notch2 Maintains Neural Stem Cell Quiescence in the Adult Hippocampus
Zhang R, Boareto M, Engler A, Louvi A, Giachino C, Iber D, Taylor V. Id4 Downstream of Notch2 Maintains Neural Stem Cell Quiescence in the Adult Hippocampus. Cell Reports 2019, 28: 1485-1498.e6. PMID: 31390563, DOI: 10.1016/j.celrep.2019.07.014.Peer-Reviewed Original ResearchConceptsNeural stem cellsDentate gyrusNSC quiescenceAdult mouse hippocampal dentate gyrusNSC proliferationMouse hippocampal dentate gyrusAdult dentate gyrusHippocampal dentate gyrusExpense of neurogenesisNeural stem cell quiescenceId4 knockdownAdult hippocampusNeuron generationId4 expressionNeuronal differentiationCell cycle entryNSC activationMajor effectorStem cell quiescenceNotch2NeurogenesisCell quiescenceStem cellsDownstream targetsNSC maintenance
2018
Notch2 Signaling Maintains NSC Quiescence in the Murine Ventricular-Subventricular Zone
Engler A, Rolando C, Giachino C, Saotome I, Erni A, Brien C, Zhang R, Zimber-Strobl U, Radtke F, Artavanis-Tsakonas S, Louvi A, Taylor V. Notch2 Signaling Maintains NSC Quiescence in the Murine Ventricular-Subventricular Zone. Cell Reports 2018, 22: 992-1002. PMID: 29386140, DOI: 10.1016/j.celrep.2017.12.094.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell DifferentiationLateral VentriclesMiceNeural Stem CellsReceptor, Notch2Signal TransductionConceptsV-SVZ neural stem cellsVentricular-subventricular zoneNeural stem cellsQuiescent neural stem cellsRostral migratory streamNew olfactory bulb neuronsNSC quiescenceOlfactory bulb neuronsLoss of Notch2Bulb neuronsNew neuronsAdult forebrainOB lineageAging-like phenotypesMigratory streamNotch2 functionNeuronsNotch2Canonical Notch signalingNeurogenesisStem cellsNotch signalingCell cycleForebrainQuiescence
2017
Disruptions in asymmetric centrosome inheritance and WDR62-Aurora kinase B interactions in primary microcephaly
Sgourdou P, Mishra-Gorur K, Saotome I, Henagariu O, Tuysuz B, Campos C, Ishigame K, Giannikou K, Quon JL, Sestan N, Caglayan AO, Gunel M, Louvi A. Disruptions in asymmetric centrosome inheritance and WDR62-Aurora kinase B interactions in primary microcephaly. Scientific Reports 2017, 7: 43708. PMID: 28272472, PMCID: PMC5341122, DOI: 10.1038/srep43708.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAurora Kinase BBrainCell CycleCell Cycle ProteinsCell DifferentiationCell ProliferationCentrosomeConsanguinityDisease Models, AnimalEpistasis, GeneticFluorescent Antibody TechniqueGene ExpressionHumansInheritance PatternsMaleMiceMice, KnockoutMicrocephalyMutationNerve Tissue ProteinsNeural Stem CellsPedigreeWhole Genome SequencingConceptsChromosome passenger complexPatient-derived fibroblastsCentrosome inheritanceNeocortical progenitorsDisease-associated mutant formsSpindle pole localizationAurora kinase BPassenger complexMitotic progressionMouse orthologDiverse functionsMutant formsWD repeat domain 62Key regulatorCPC componentsKinase BPole localizationPrimary microcephalyLate neurogenesisRecessive mutationsNeuronal differentiationWDR62Severe brain malformationsReduced proliferationNeocortical development
2014
Mutations in KATNB1 Cause Complex Cerebral Malformations by Disrupting Asymmetrically Dividing Neural Progenitors
Mishra-Gorur K, Çağlayan AO, Schaffer AE, Chabu C, Henegariu O, Vonhoff F, Akgümüş GT, Nishimura S, Han W, Tu S, Baran B, Gümüş H, Dilber C, Zaki MS, Hossni HA, Rivière JB, Kayserili H, Spencer EG, Rosti RÖ, Schroth J, Per H, Çağlar C, Çağlar Ç, Dölen D, Baranoski JF, Kumandaş S, Minja FJ, Erson-Omay EZ, Mane SM, Lifton RP, Xu T, Keshishian H, Dobyns WB, C. N, Šestan N, Louvi A, Bilgüvar K, Yasuno K, Gleeson JG, Günel M. Mutations in KATNB1 Cause Complex Cerebral Malformations by Disrupting Asymmetrically Dividing Neural Progenitors. Neuron 2014, 84: 1226-1239. PMID: 25521378, PMCID: PMC5024344, DOI: 10.1016/j.neuron.2014.12.014.Peer-Reviewed Original ResearchConceptsComplex cerebral malformationsCerebral cortical malformationsMicrotubule-severing enzyme kataninExome sequencing analysisMitotic spindle formationDrosophila optic lobeCerebral malformationsPatient-derived fibroblastsCell cycle progression delayCortical malformationsMotor neuronsComplex malformationsMicrotubule-associated proteinsCortical developmentReduced cell numberOptic lobeRegulatory subunitBrain developmentCatalytic subunitDeleterious mutationsSpindle formationSupernumerary centrosomesArborization defectsMalformationsHuman phenotypesCcm3, a gene associated with cerebral cavernous malformations, is required for neuronal migration
Louvi A, Nishimura S, Günel M. Ccm3, a gene associated with cerebral cavernous malformations, is required for neuronal migration. Development 2014, 141: 1404-1415. PMID: 24595293, PMCID: PMC3943187, DOI: 10.1242/dev.093526.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosis Regulatory ProteinsCell MovementCell ProliferationCyclin-Dependent Kinase 5FemaleHemangioma, Cavernous, Central Nervous SystemIntracellular Signaling Peptides and ProteinsMiceMice, KnockoutMice, TransgenicNeocortexNeural Stem CellsNeurogliaPregnancyRho GTP-Binding ProteinsRhoA GTP-Binding ProteinSignal TransductionConceptsCerebral cavernous malformation 3Neuronal migrationCerebral cavernous malformationsRadial glia progenitorsCell non-autonomous functionCerebrovascular disordersPyramidal neuronsCortical plateLaminar positioningSubventricular zoneCortical developmentCavernous malformationsRadial gliaLoss of functionNascent neuronsNeuronal morphologySevere malformationsGlia progenitorsNeural progenitorsNeuronsNon-autonomous functionsMalformationsRhoA pathwayPossible interactionsGlia