Search results for "chromosome"

showing 10 items of 1175 documents

Preservation of genetic and regulatory robustness in ancient gene duplicates of Saccharomyces cerevisiae

2014

[EN] Biological systems remain robust against certain genetic and environmental challenges. Robustness allows the exploration of ecological adaptations. It is unclear what factors contribute to increasing robustness. Gene duplication has been considered to increase genetic robustness through functional redundancy, accelerating the evolution of novel functions. However, recent findings have questioned the link between duplication and robustness. In particular, it remains elusive whether ancient duplicates still bear potential for innovation through preserved redundancy and robustness. Here we have investigated this question by evolving the yeast Saccharomyces cerevisiae for 2200 generations …

DNA Mutational AnalysisGenes FungalSaccharomyces cerevisiaeSaccharomyces cerevisiaeBiologyPolymorphism Single NucleotideGenome03 medical and health sciences0302 clinical medicineINDEL MutationStress PhysiologicalGene DuplicationGene duplicationDNA Mutational AnalysisGeneticsBiologyGeneGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesModels GeneticResearchFungal geneticsRobustness (evolution)biology.organism_classificationAdaptation PhysiologicalPhenotypeEvolutionary biologyMutationChromosomes FungalDirected Molecular EvolutionGenome FungalAlgorithms030217 neurology & neurosurgeryGenome Research
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Cell proliferation and DNA breaks are involved in ultraviolet light-induced apoptosis in nucleotide excision repair-deficient Chinese hamster cells.

2002

UV light targets both membrane receptors and nuclear DNA, thus evoking signals triggering apoptosis. Although receptor-mediated apoptosis has been extensively investigated, the role of DNA damage in apoptosis is less clear. To analyze the importance of DNA damage induced by UV-C light in apoptosis, we compared nucleotide excision repair (NER)-deficient Chinese hamster ovary cells (lines 27-1 and 43-3B mutated for the repair genes ERCC3 and ERCC1, respectively) with the corresponding DNA repair-proficient fibroblasts (CHO-9 and ERCC1 complemented 43-3B cells). NER-deficient cells were hypersensitive as to the induction of apoptosis, indicating that apoptosis induced by UV-C light is due to u…

DNA RepairTranscription GeneticDNA repairDNA damageCell SurvivalUltraviolet RaysApoptosisCHO CellsBiologyCysteine Proteinase InhibitorsRadiation ToleranceArticleMiceCricetinaeUltraviolet lightAnimalsMolecular BiologyChromosome AberrationsIntrinsic apoptosisCell CycleDNA replicationCell BiologyFibroblastsMolecular biologyCaspase InhibitorsChromatinCell biologyKineticsUVB-induced apoptosisProto-Oncogene Proteins c-bcl-2ApoptosisMutationTumor Suppressor Protein p53Cell DivisionNucleotide excision repairDNA DamageMolecular biology of the cell
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Excision of Uracil from Transcribed DNA Negatively Affects Gene Expression

2014

Uracil is an unavoidable aberrant base in DNA, the repair of which takes place by a highly efficient base excision repair mechanism. The removal of uracil from the genome requires a succession of intermediate products, including an abasic site and a single strand break, before the original DNA structure can be reconstituted. These repair intermediates are harmful for DNA replication and also interfere with transcription under cell-free conditions. However, their relevance for cellular transcription has not been proved. Here we investigated the influence of uracil incorporated into a reporter vector on gene expression in human cells. The expression constructs contained a single uracil opposi…

DNA RepairTranscription GeneticGreen Fluorescent ProteinsGene ExpressionDNA and ChromosomesBiologyBiochemistryCell LineDNA Glycosylaseschemistry.chemical_compoundGenes ReporterActivation-induced (cytidine) deaminaseHumansheterocyclic compoundsProtein–DNA interactionAP siteUracilUracil-DNA GlycosidaseMolecular BiologyUracilDNACell BiologyBase excision repairMolecular biologyThymine DNA GlycosylasechemistryDNA glycosylaseGene Knockdown TechniquesUracil-DNA glycosylasebiology.proteinHeLa CellsNucleotide excision repairJournal of Biological Chemistry
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Mechanisms and consequences of methylating agent-induced SCEs and chromosomal aberrations: a long road traveled and still a far way to go.

2003

Since the milestone work of Evans and Scott, demonstrating the replication dependence of alkylation-induced aberrations, and Obe and Natarajan, pointing to the critical role of DNA double-strand breaks (DSBs) as the ultimate trigger of aberrations, the field has grown extensively. A notable example is the identification of DNA methylation lesions provoking chromosome breakage (clastogenic) effects, which made it possible to model clastogenic pathways evoked by genotoxins. Experiments with repair-deficient mutants and transgenic cell lines revealed both O<sup>6</sup>-methylguanine (O<sup>6</sup>MeG) and N- methylpurines as critical lesions. For S<sub>N</sub&g…

DNA ReplicationAlkylating AgentsGuanineDNA RepairDNA damageDNA repairBase Pair MismatchApoptosisBiologyMethylationLesionAnimals Genetically ModifiedMiceO(6)-Methylguanine-DNA MethyltransferaseCricetulusCricetinaeGeneticsmedicineAnimalsHumansPoint MutationAP siteMolecular BiologyGenetics (clinical)Chromosome AberrationsRecombination GeneticGuanosineModels GeneticCell CycleDNA replicationDNAFibroblastsMolecular biologyCell killingCell Transformation NeoplasticCancer researchDNA mismatch repairChromosome breakagemedicine.symptomSister Chromatid ExchangeDNA DamageMutagensCytogenetic and genome research
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Functional Inactivation of pRB Results in Aneuploid Mammalian Cells After Release From a Mitotic Block

2002

AbstractThe widespread chromosome instability observed in tumors and in early stage carcinomas suggests that aneuploidy could be a prerequisite for cellular transformation and tumor initiation. Defects in tumor suppressers and genes that are part of mitotic checkpoints are likely candidates for the aneuploid phenotype. By using flow cytometric, cytogenetic, immunocytochemistry techniques we investigated whether pRB deficiency could drive perpetual aneuploidy in normal human and mouse fibroblasts after mitotic checkpoint challenge by microtubule-destabilizing drugs. Both mouse and human pRB-deficient primary fibroblasts resulted, upon release from a mitotic block, in proliferating aneuploid …

DNA ReplicationCancer ResearchBrief ArticleClone (cell biology)MitosisAneuploidyCre recombinaseSpindle Apparatuslcsh:RC254-282Retinoblastoma ProteinColony-Forming Units AssayMicechemistry.chemical_compoundChromosome instabilitymedicineAnimalsHumanscentrosomesCINGenes RetinoblastomaMitosisCells CulturedIn Situ Hybridization FluorescenceCentrosomeCell cycle controlbiologyColcemidChromosome FragilityCell CycleGINDemecolcineRetinoblastoma proteinAneuploidy; Cell cycle control; Centrosomes; CIN; PRB;FibroblastsCell cyclelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensAneuploidyFlow Cytometrymedicine.diseaseAntineoplastic Agents PhytogenicCell biologyCell Transformation NeoplasticPRBMicroscopy Fluorescencechemistrybiology.proteinFemaleNeoplasia
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The high rate of endoreduplication in the repair deficient CHO mutant EM9 parallels a reduced level of methylated deoxycytidine in DNA

2008

It has been recently proposed that hypomethylation of DNA induced by 5-azacytidine (5-azaC) leads to reduced chromatid decatenation that ends up in endoreduplication, most likely due to a failure in topo II function [S. Mateos, I. Domínguez, N. Pastor, G. Cantero, F. Cortés, The DNA demethylating 5-azaC induces endoreduplication in cultured Chinese hamster cells, Mutat. Res. 578 (2005) 33-42]. The Chinese hamster mutant cell line EM9 has a high spontaneous frequency of endoreduplication as compared to its parental line AA8. In order to see if this is related to the degree of DNA methylation, we have investigated the basal levels of both endpoints in AA8 and EM9, as well as the effect of ext…

DNA ReplicationDNA RepairHealth Toxicology and MutagenesisMutantCHO CellsChromosome segregationamedicine.disease_causeDeoxycytidineChromosomesChinese hamsterHypomethylation of DNAchemistry.chemical_compoundCricetulusCricetinaeGeneticsmedicineAnimalsEndoreduplicationMolecular BiologyMutationbiologyChinese hamster ovary cellEndoreduplicationDNA Methylationbiology.organism_classificationTopoisomerase IIMolecular biologychemistryMutationDNA methylationAzacitidineChromatidDNAMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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DNA polymeraseθ up-regulation is associated with poor survival in breast cancer, perturbs DNA replication, and promotes genetic instability

2010

“Replicative stress” is one of the main factors underlying neoplasia from its early stages. Genes involved in DNA synthesis may therefore represent an underexplored source of potential prognostic markers for cancer. To this aim, we generated gene expression profiles from two independent cohorts (France,n= 206; United Kingdom,n= 117) of patients with previously untreated primary breast cancers. We report here that among the 13 human nuclear DNA polymerase genes, DNA Polymerase θ (POLQ) is the only one significantly up-regulated in breast cancer compared with normal breast tissues. Importantly,POLQup-regulation significantly correlates with poor clinical outcome (4.3-fold increased risk of de…

DNA ReplicationGenome instabilityDNA damageDNA polymerase[SDV]Life Sciences [q-bio]DNA Polymerase ThetaBreast NeoplasmsDNA-Directed DNA PolymeraseKaplan-Meier Estimatemedicine.disease_causeBioinformaticsGenomic InstabilityCell LineCohort Studies03 medical and health sciences0302 clinical medicineBreast cancerCell Line TumorChromosome instabilityCyclin EmedicineHumansComputingMilieux_MISCELLANEOUS030304 developmental biology0303 health sciencesMultidisciplinarybiologyReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingCancerMiddle AgedBiological SciencesPrognosismedicine.diseaseUnited KingdomUp-RegulationGene Expression Regulation Neoplastic030220 oncology & carcinogenesisCancer researchbiology.proteinFemaleRNA InterferenceFranceCarcinogenesisDNA DamageProceedings of the National Academy of Sciences
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Asynchronous replication dynamics of imprinted and non-imprinted chromosome regions in early mouse embryos.

2008

We have used interphase FISH to analyze the replication behavior of four imprinted chromosome regions (Snrpn, Zim1-Peg3, Dlk1-Gtl2, and Igf2r) and five non-imprinted regions in mouse one-cell to morula-stage embryos and embryonic fibroblasts. In general, imprinted chromosome regions showed the expected asynchronous pattern of replication throughout all analyzed stages of preimplantation development and in differentiated cells. The Dlk1-Gtl2 locus which is not expressed and Igf2r which is biallelically expressed in early embryos showed a relaxation of replication asynchrony at the morula stage. Asynchronous replication in zygotes and two-cell embryos was not specific to imprinted regions. Th…

DNA ReplicationMaleTranscriptional ActivationRNA UntranslatedTime FactorsSomatic cellZygoteEmbryonic DevelopmentLocus (genetics)BiologyGenomeMorulaChromosomesGenomic InstabilityEpigenesis GeneticGenomic ImprintingMiceChromosome regionsAnimalsImprinting (psychology)GeneCells CulturedIn Situ Hybridization FluorescenceGeneticsZygoteChromosome MappingCell BiologyEmbryo MammalianMice Inbred C57BLFertilizationembryonic structuresFemalePloidyCell DivisionExperimental cell research
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Chromosomal instability, reproductive cell death and apoptosis induced by O6-methylguanine in Mex−, Mex+ and methylation-tolerant mismatch repair com…

1998

O6-Methylguanine (O6-MeG) is induced in DNA by methylating environmental carcinogens and various cytostatic drugs. It is repaired by O6-methylguanine-DNA methyltransferase (MGMT). If not repaired prior to replication, the lesion generates gene mutations and leads to cell death, sister chromatid exchanges (SCEs), chromosomal aberrations and malignant transformation. To address the question of how O6-MeG is transformed into genotoxic effects, isogenic Chinese hamster cell lines either not expressing MGMT (phenotypically Mex-), expressing MGMT (Mex+) or exhibiting the tolerance phenotype (Mex-, methylation resistant) were compared as to their clastogenic response. Mex- cells were more sensitiv…

DNA ReplicationMethylnitronitrosoguanidineGuanineDNA RepairDNA damageHealth Toxicology and MutagenesisDrug ResistanceApoptosisCHO CellsGene mutationBiologyChromosomesDNA AdductsO(6)-Methylguanine-DNA MethyltransferaseCricetulusCricetinaeChromosome instabilityGeneticsAnimalsSister chromatidsMolecular BiologyMitosisChromosome AberrationsCell DeathModels GeneticMutagenicity TestsDNA replicationDNA MethylationMolecular biologyDNA methylationDNA mismatch repairSister Chromatid ExchangeMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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Replication origins and pause sites in sea urchin mitochondrial DNA

1992

We have used a combination of one- and two-dimensional agarose gel electrophoresis, and solution hybridization to strand-specific probes, to map the replication origin of sea urchin mitochondrial DNA and to investigate the structure of replication intermediates. These assays are consistent with replication initiating unidirectionally from the D-loop region by D-loop expansion, as in vertebrates. A prominent site of initiation of lagging-strand synthesis lies at, or near to, the boundary between the genes for ATPase 6 and COIII, which is also close to a pause site for leading-strand synthesis. These findings suggest a role for pause sites in the regulation of mitochondrial transcription and …

DNA ReplicationMitochondrial DNAMacromolecular SubstancesRestriction MappingEukaryotic DNA replicationBiologyOrigin of replicationPre-replication complexDNA MitochondrialDNA RibosomalGeneral Biochemistry Genetics and Molecular BiologyElectron Transport Complex IVRNA TransferControl of chromosome duplicationAnimalsElectrophoresis Gel Two-DimensionalGeneral Environmental ScienceElectrophoresis Agar GelGeneral Immunology and MicrobiologyTer proteinChromosome MappingNADH DehydrogenaseGeneral MedicineMolecular biologyCell biologyRNA RibosomalSea UrchinsNucleic Acid ConformationOrigin recognition complexSolution hybridizationGeneral Agricultural and Biological SciencesProceedings of the Royal Society of London. Series B: Biological Sciences
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