2024
Multiple mechanisms for licensing human replication origins
Yang R, Hunker O, Wise M, Bleichert F. Multiple mechanisms for licensing human replication origins. Nature 2024, 636: 488-498. PMID: 39604729, PMCID: PMC11910750, DOI: 10.1038/s41586-024-08237-8.Peer-Reviewed Original ResearchOrigin recognition complexReplication originsMCM loadingHexamer formationDNA replication initiationDNA replication machineryHuman replication originsOrc6 subunitMulticellular eukaryotesBiochemical reconstitutionReplication initiationRecognition complexReplicative helicaseMultiple mechanismsReplication machineryEukaryotic MCM2Helicase motorReplication stressOrigin licensingDimer interfaceOrc6Reconstituted systemYeastHexamerMCM2
2022
A mechanism of origin licensing control through autoinhibition of S. cerevisiae ORC·DNA·Cdc6
Schmidt JM, Yang R, Kumar A, Hunker O, Seebacher J, Bleichert F. A mechanism of origin licensing control through autoinhibition of S. cerevisiae ORC·DNA·Cdc6. Nature Communications 2022, 13: 1059. PMID: 35217664, PMCID: PMC8881611, DOI: 10.1038/s41467-022-28695-w.Peer-Reviewed Original ResearchConceptsOrigin recognition complexS. cerevisiaeCyclin-dependent kinase phosphorylationMcm2-7 loadingN-terminal domainCryo-electron microscopyCDK phosphorylationRecognition complexDNA replicationReplication originsÅ resolutionKinase phosphorylationMechanism of originCdc6Coordinated actionCerevisiaePhosphorylationDNAInhibitory signalsStructural detailsSite regulationRecruitmentOrc6AssemblyCdt1
2020
Structural mechanism for replication origin binding and remodeling by a metazoan origin recognition complex and its co-loader Cdc6
Schmidt JM, Bleichert F. Structural mechanism for replication origin binding and remodeling by a metazoan origin recognition complex and its co-loader Cdc6. Nature Communications 2020, 11: 4263. PMID: 32848132, PMCID: PMC7450096, DOI: 10.1038/s41467-020-18067-7.Peer-Reviewed Original ResearchMeSH KeywordsAAA DomainAdenosine TriphosphateAnimalsCell Cycle ProteinsCryoelectron MicroscopyDNADrosophila melanogasterDrosophila ProteinsHydrolysisMinichromosome Maintenance ProteinsModels, MolecularOrigin Recognition ComplexProtein BindingRecombinant ProteinsReplication OriginSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsConceptsOrigin recognition complexRecognition complexReplication originsDrosophila origin recognition complexEukaryotic DNA replication initiationMetazoan origin recognition complexCryo-electron microscopy structureMcm2-7 replicative helicaseATPase siteDNA replication initiationWalker B motifMcm2-7 loadingWinged-helix domainReplicative helicaseReplication initiationMicroscopy structureDistinct DNAB motifOrigin recognitionDNA sequencesDNA bendingDNA bindingPrimary DNADNA geometryLoop region
2019
H2A.Z facilitates licensing and activation of early replication origins
Long H, Zhang L, Lv M, Wen Z, Zhang W, Chen X, Zhang P, Li T, Chang L, Jin C, Wu G, Wang X, Yang F, Pei J, Chen P, Margueron R, Deng H, Zhu M, Li G. H2A.Z facilitates licensing and activation of early replication origins. Nature 2019, 577: 576-581. PMID: 31875854, DOI: 10.1038/s41586-019-1877-9.Peer-Reviewed Original ResearchConceptsOrigin recognition complexHistone variant H2A.ZEarly replication originsReplication originsVariant H2A.ZReplication timingChromatin-based regulatory mechanismsEarly replication timingGenome-wide studiesNascent DNA strandsH2A.Z resultsNucleosome bindsDNA replicationH2A.ZHistone H4Cell cycle1Precise duplicationRegulated processDNA sequencesRegulatory mechanismsHeLa cellsDNA strandsORC1Firing efficiencyGenomeOrigins of DNA replication
Ekundayo B, Bleichert F. Origins of DNA replication. PLOS Genetics 2019, 15: e1008320. PMID: 31513569, PMCID: PMC6742236, DOI: 10.1371/journal.pgen.1008320.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsKingdoms of lifeDomains of lifeDaughter cellsDNA replicationReplication originsCell divisionAccurate duplicationDaughter strandsGenomic DNAHereditary informationSemiconservative replicationGenetic materialFull complementDNA synthesisDiscrete sitesDNABidirectional mannerReplicationDivergent strategiesChromosomesOrganismsDuplicationOriginCellsStrands
2015
NUCKS1 is a novel RAD51AP1 paralog important for homologous recombination and genome stability
Parplys AC, Zhao W, Sharma N, Groesser T, Liang F, Maranon DG, Leung SG, Grundt K, Dray E, Idate R, Østvold AC, Schild D, Sung P, Wiese C. NUCKS1 is a novel RAD51AP1 paralog important for homologous recombination and genome stability. Nucleic Acids Research 2015, 43: 9817-9834. PMID: 26323318, PMCID: PMC4787752, DOI: 10.1093/nar/gkv859.Peer-Reviewed Original ResearchConceptsHomologous recombinationDNA replication fork progressionChromatin-associated proteinsVertebrate-specific proteinReplication fork progressionDNA damage responseDNA repair pathwaysNew replication originsNumber of proteinsExtensive sequence homologyImpairs DNA repairGenome stabilityLimited functional dataChromosome stabilityFork progressionDamage responseReplication originsHR pathwayPhenotypic effectsDNA repairRepair pathwaysSequence homologyTumor suppressionSame DNANUCKS1Embryonic Stem Cells License a High Level of Dormant Origins to Protect the Genome against Replication Stress
Ge XQ, Han J, Cheng EC, Yamaguchi S, Shima N, Thomas JL, Lin H. Embryonic Stem Cells License a High Level of Dormant Origins to Protect the Genome against Replication Stress. Stem Cell Reports 2015, 5: 185-194. PMID: 26190528, PMCID: PMC4618655, DOI: 10.1016/j.stemcr.2015.06.002.Peer-Reviewed Original ResearchConceptsEmbryonic stem cellsStem/progenitor cellsNeural stem/progenitor cellsStem cellsProgenitor cellsTissue stem/progenitor cellsMCM2-7 complexDNA replication originsTissue-specific stem/progenitor cellsStem cell typesGenome integrityGenomic integrityReplication stressDormant originsReplication forksReplicative stressDNA replicationReplication originsNeural lineagesDNA damageS phaseCell typesAbnormal neurogenesisCellsGenome
2012
Some Novel Insights on HPV16 Related Cervical Cancer Pathogenesis Based on Analyses of LCR Methylation, Viral Load, E7 and E2/E4 Expressions
Ghosh D, Bhattacharjee B, Sen S, Premi L, Mukhopadhyay I, Chowdhury R, Roy S, Sengupta S. Some Novel Insights on HPV16 Related Cervical Cancer Pathogenesis Based on Analyses of LCR Methylation, Viral Load, E7 and E2/E4 Expressions. PLOS ONE 2012, 7: e44678. PMID: 22970286, PMCID: PMC3435323, DOI: 10.1371/journal.pone.0044678.Peer-Reviewed Original ResearchConceptsLong control regionViral loadViral genomeReplication originsCaCx casesEpisomal HPV16 genomesLack of methylationE7 mRNA expressionHuman papillomavirus 16Binding site IGene copy numberCervical cancer pathogenesisRepressor proteinBisulphite sequencingControl regionHPV16 genomeCervical carcinogenesisHost genesGenomeCervical cancerCopy numberViral transcriptionHPV16Cancer pathogenesisOncogene E7
1980
Cold-sensitive regulatory mutants of simian virus 40
DiMaio D, Nathans D. Cold-sensitive regulatory mutants of simian virus 40. Journal Of Molecular Biology 1980, 140: 129-142. PMID: 6251230, DOI: 10.1016/0022-2836(80)90359-9.Peer-Reviewed Original ResearchConceptsRegulatory segmentBase substitutionsBglI siteWild-type plaquesProtein-coding sequencesProtein-nucleic acid interactionsCold-sensitive mutantsOrigin of replicationSet of mutantsSimian virus 40 mutantsDNA polymerase IBase substitution mutationsRNA processingRegulatory mutantsDNA replicationReplication originsViable mutantsSimian virus 40Small plaquesMutational alterationsWild-type virusPolymerase IMutantsRegulatory phenomenaSubstitution mutations
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