Dan Doyle
Postdoctoral Fellow in the Child Study CenterAbout
Research
Publications
2022
Postmitotic accumulation of histone variant H3.3 in new cortical neurons establishes neuronal chromatin, transcriptome, and identity
Funk O, Qalieh Y, Doyle D, Lam M, Kwan K. Postmitotic accumulation of histone variant H3.3 in new cortical neurons establishes neuronal chromatin, transcriptome, and identity. Proceedings Of The National Academy Of Sciences Of The United States Of America 2022, 119: e2116956119. PMID: 35930666, PMCID: PMC9371731, DOI: 10.1073/pnas.2116956119.Peer-Reviewed Original ResearchConceptsNeuronal chromatinHistone variantsVariant H3.3Histone H3 variant H3.3Replication-coupled depositionHistone variant H3.3Replication-dependent histonesKey developmental roleNucleosome turnoverNeural progenitor cellsChromatin stateHistone replacementNeuronal transcriptomeModification landscapeDevelopmental phenotypesGene regulationTranscriptional disruptionH3.3Neuronal lifespanCellular phenotypesHistone H3 levelsNeuronal identityDevelopmental roleTranscriptomePostmitotic cellsNeurogenic–angiogenic synchrony via lactate
Doyle D, Kwan K. Neurogenic–angiogenic synchrony via lactate. Nature Neuroscience 2022, 25: 839-840. PMID: 35788196, DOI: 10.1038/s41593-022-01111-8.Peer-Reviewed Original Research
2021
Chromatin remodeler Arid1a regulates subplate neuron identity and wiring of cortical connectivity
Doyle D, Lam M, Qalieh A, Qalieh Y, Sorel A, Funk O, Kwan K. Chromatin remodeler Arid1a regulates subplate neuron identity and wiring of cortical connectivity. Proceedings Of The National Academy Of Sciences Of The United States Of America 2021, 118: e2100686118. PMID: 34011608, PMCID: PMC8166177, DOI: 10.1073/pnas.2100686118.Peer-Reviewed Original ResearchMeSH KeywordsAbnormalities, MultipleAnimalsCerebral CortexChromatinConnectomeCorpus CallosumDNA-Binding ProteinsFaceGene DeletionGene Expression RegulationGray MatterHand Deformities, CongenitalHumansIntellectual DisabilityLoss of Function MutationMiceMice, TransgenicMicrognathismNeckNeural PathwaysNeuronsThalamusTranscription FactorsVibrissaeWhite MatterConceptsSubplate neuronsCorpus callosumThalamocortical Axon TargetingNeural circuit wiringCoffin-Siris syndromeSubplate ablationThalamocortical neuronsCallosal axonsAscending axonsBarrel developmentIntracortical axonsCortical developmentCortical connectivityWhite matterAxon targetingWhisker barrelsSelective lossNeuron identityExtracellular matrixAxonsCircuit wiringFunction mutationsCallosumAxon guidanceDevelopmental disorders
2020
Symmetric neural progenitor divisions require chromatin-mediated homologous recombination DNA repair by Ino80
Keil J, Doyle D, Qalieh A, Lam M, Funk O, Qalieh Y, Shi L, Mohan N, Sorel A, Kwan K. Symmetric neural progenitor divisions require chromatin-mediated homologous recombination DNA repair by Ino80. Nature Communications 2020, 11: 3839. PMID: 32737294, PMCID: PMC7395731, DOI: 10.1038/s41467-020-17551-4.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisATPases Associated with Diverse Cellular ActivitiesBRCA2 ProteinCell DivisionChromatinChromatin Assembly and DisassemblyDNADNA Breaks, Double-StrandedDNA-Binding ProteinsEmbryo, MammalianGene Expression Regulation, DevelopmentalMiceMice, TransgenicNeocortexNeural Stem CellsNeurogenesisRecombinational DNA RepairSignal TransductionTumor Suppressor Protein p53YY1 Transcription FactorConceptsHomologous recombination DNA repairDNA repairIno80 deletionNeural progenitor cellsChromatin-mediated transcriptional regulationDNA double-strand break repairDouble-strand break repairSpatiotemporal gene expressionLoss of INO80HR DNA repairUnrepaired DNA breaksAsymmetric neurogenic divisionsNeural progenitor divisionsDNA damage repairP53-dependent apoptosisINO80 functionGenome maintenanceTranscriptional regulationINO80Break repairDNA breaksProgenitor divisionsDamage repairGene expressionNPC division
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