Search results for "Gene duplication"

showing 10 items of 153 documents

Microcephaly/Trigonocephaly, Intellectual Disability, Autism Spectrum Disorder, and Atypical Dysmorphic Features in a Boy with Xp22.31 Duplication

2019

The Xp22.31 segment of the short arm of the human X chromosome is a region of high instability with frequent rearrangement. The duplication of this region has been found in healthy people as well as in individuals with varying degrees of neurological impairment. The incidence has been reported in a range of 0.4-0.44% of the patients with neurological impairment. Moreover, there is evidence that Xp22.31 duplication may cause a common phenotype including developmental delay, intellectual disability, feeding difficulty, autistic spectrum disorders, hypotonia, seizures, and talipes. We report on a patient with microcephaly and trigonocephaly, moderate intellectual disability, speech and languag…

0301 basic medicinePediatricsmedicine.medical_specialtyMicrocephalyLanguage delayDevelopmental delayTrigonocephaly030105 genetics & heredityTooth anomaliesXp22.31 duplication03 medical and health sciencesGene duplicationIntellectual disabilityGeneticsmedicineTrigonocephalyTooth anomaliePathologicalGenetics (clinical)business.industrymedicine.diseaseHypotoniaAutism spectrum disorderNovel Insights from Clinical PracticeMicrocephalymedicine.symptombusiness
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7q31.32 partial duplication: First report of a child with dysmorphism, autistic spectrum disorder, moderate intellectual disability and, epilepsy. Li…

2019

Abstract Introduction Duplication of long arm of chromosome 7(q) is uncommon. It may occur as “pure”, isolated anomaly or in association with other mutations involving the same or other chromosomes. “Pure” chromosome 7q duplication has recently been classified by segment involved: the interstitial, proximal, or distal segment of the arm. Attempts to correlate genotype with phenotype in each group has yielded questionable results even though intellective disability and minor dysmorphic features of variable types are typically seen. Material and Methods In a young boy showing minor facial dysmorphism, language delay, autistic spectrum disorder, epileptic seizures, behavioral disturbances and …

0301 basic medicineProbandPediatricsmedicine.medical_specialtyAutism Spectrum DisorderLanguage delayDevelopmental DisabilitiesIrritabilityChromosomes03 medical and health sciencesEpilepsy0302 clinical medicineIntellectual DisabilityGene duplicationIntellectual disabilityHumansMedicineGenetic Association StudiesChromosome 7 (human)Epilepsybusiness.industrymedicine.disease7q31.32 duplicationDysmorphism030104 developmental biologyAutistic spectrum disorderNeurologyAutism spectrum disorderPair 7Neurology (clinical)medicine.symptombusinessChromosomes Human Pair 7030217 neurology & neurosurgeryHumanEpilepsy Research
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De novoassembly of the zucchini genome reveals a whole-genome duplication associated with the origin of theCucurbitagenus

2018

Summary The Cucurbita genus (squashes, pumpkins and gourds) includes important domesticated species such as C. pepo, C. maxima and C. moschata. In this study, we present a high-quality draft of the zucchini (C. pepo) genome. The assembly has a size of 263 Mb, a scaffold N50 of 1.8 Mb and 34 240 gene models. It includes 92% of the conserved BUSCO core gene set, and it is estimated to cover 93.0% of the genome. The genome is organized in 20 pseudomolecules that represent 81.4% of the assembly, and it is integrated with a genetic map of 7718 SNPs. Despite the small genome size, three independent lines of evidence support that the C. pepo genome is the result of a whole-genome duplication: the …

0301 basic medicineSequence assemblyPlant ScienceBiologyBiotecnologiaGenome03 medical and health sciencesCucurbitaGene DuplicationGene duplicationGene familycropCucurbitagenomeGenome sizeGeneCitrullusResearch Articlesbiology.organism_classificationBiological EvolutionzucchiniCucurbitaceaeGenòmica030104 developmental biologyEvolutionary biologywhole‐genome duplicationTranscriptomeAgronomy and Crop ScienceGenome PlantResearch ArticleBiotechnologyPlant Biotechnology Journal
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Genome Mutational and Transcriptional Hotspots Are Traps for Duplicated Genes and Sources of Adaptations

2017

Gene duplication generatesnewgeneticmaterial,which has been shownto lead tomajor innovations in unicellular andmulticellular organisms.Awhole-genome duplication occurred in the ancestor of Saccharomyces yeast species but 92%of duplicates returned to single-copy genes shortly after duplication. The persisting duplicated genes in Saccharomyces led to the origin of major metabolic innovations, which have been the source of the unique biotechnological capabilities in the Baker's yeast Saccharomyces cerevisiae. What factors have determined the fate of duplicated genes remains unknown. Here,we report the first demonstration that the local genome mutation and transcription rates determine the fate…

0301 basic medicineTranscription GeneticGene duplicationAdaptation BiologicalSaccharomyces cerevisiaeEnvironmental stressPhenotypic plasticityBiologyGenomeEnvironmental stressMutational genome hotspots03 medical and health sciencesMutation RateStress PhysiologicalGene duplicationGeneticsPromoter Regions GeneticEcology Evolution Behavior and SystematicsGeneticsAdaptationsGenetic redundancyDuplicated genes030104 developmental biologyMutationGenetic redundancyExpression genome hotspotsResearch Article
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Evaluation of DNA Methylation Episignatures for Diagnosis and Phenotype Correlations in 42 Mendelian Neurodevelopmental Disorders

2020

Contains fulltext : 218274.pdf (Publisher’s version ) (Closed access) Genetic syndromes frequently present with overlapping clinical features and inconclusive or ambiguous genetic findings which can confound accurate diagnosis and clinical management. An expanding number of genetic syndromes have been shown to have unique genomic DNA methylation patterns (called "episignatures"). Peripheral blood episignatures can be used for diagnostic testing as well as for the interpretation of ambiguous genetic test results. We present here an approach to episignature mapping in 42 genetic syndromes, which has allowed the identification of 34 robust disease-specific episignatures. We examine emerging pa…

0301 basic medicine[SDV]Life Sciences [q-bio]Computational biology030105 genetics & heredityBiologyPediatricsArticleCohort Studiesmolecular diagnostics03 medical and health sciencessymbols.namesakeGenetic HeterogeneityGene duplicationGeneticsHumansHunter-McAlpine syndromeGenetics (clinical)Mass screening030304 developmental biologyEpiSignGenetics0303 health sciencesNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]DNA methylationGenetic heterogeneity030305 genetics & heredityCorrectionSyndromeDNA MethylationMolecular diagnosticsPhenotypePenetranceHuman genetics3. Good healthepisignaturegenomic DNA030104 developmental biologyPhenotypeNeurodevelopmental DisordersDNA methylationuncertain clinical casesMendelian inheritancesymbolsIdentification (biology)VUS classification
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Co-regulation of paralog genes in the three-dimensional chromatin architecture.

2016

Paralog genes arise from gene duplication events during evolution, which often lead to similar proteins that cooperate in common pathways and in protein complexes. Consequently, paralogs show correlation in gene expression whereby the mechanisms of co-regulation remain unclear. In eukaryotes, genes are regulated in part by distal enhancer elements through looping interactions with gene promoters. These looping interactions can be measured by genome-wide chromatin conformation capture (Hi-C) experiments, which revealed self-interacting regions called topologically associating domains (TADs). We hypothesize that paralogs share common regulatory mechanisms to enable coordinated expression acco…

0301 basic medicineanimal structuresComputational biologyBiologyGenomeChromosome conformation capture03 medical and health sciencesMice0302 clinical medicineDogsGene DuplicationGene duplicationGeneticsAnimalsCluster AnalysisHumansPromoter Regions GeneticGeneChIA-PETGenomic organizationGeneticsRegulation of gene expressionGenomefungiGene regulation Chromatin and EpigeneticsComputational BiologyChromatin Assembly and DisassemblyBiological EvolutionChromatinChromatin030104 developmental biologyEnhancer Elements GeneticGene Expression Regulation030217 neurology & neurosurgeryNucleic acids research
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Leukemia-associated activating mutation of Flt3 expands dendritic cells and alters T cell responses

2016

Lau et al. show that the FLT3-ITD mutation directly affects dendritic cell development in preleukemic mice, indirectly modulating T cell homeostasis and supporting the expansion of regulatory T cells.

0301 basic medicinemedicine.medical_treatmentT cellT-LymphocytesImmunologyDown-RegulationBiologyCD8-Positive T-LymphocytesArticle03 medical and health sciences0302 clinical medicinehemic and lymphatic diseasesGene DuplicationmedicineImmunology and AllergyAnimalsHomeostasisCell LineageProgenitor cellResearch ArticlesCell ProliferationLeukemiaCell growthGene Expression Regulation LeukemicMyeloid leukemiaMembrane Proteinshemic and immune systemsDendritic CellsCell biologyImmunosurveillanceMice Inbred C57BLHaematopoiesis030104 developmental biologyCytokinemedicine.anatomical_structureImmunologyMutationCD8030215 immunologySignal TransductionThe Journal of Experimental Medicine
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Graph-based network analysis of transcriptional regulation pattern divergence in duplicated yeast gene pairs

2019

The genome and interactome of Saccharomyces cerevisiae have been characterized extensively over the course of the past few decades. However, despite many insights gained over the years, both functional studies and evolutionary analyses continue to reveal many complexities and confounding factors in the construction of reliable transcriptional regulatory network models. We present here a graph-based technique for comparing transcriptional regulatory networks based on network motif similarity for gene pairs. We construct interaction graphs for duplicated transcription factor pairs traceable to the ancestral whole-genome duplication as well as other paralogues in Saccharomyces cerevisiae. We c…

0303 health sciencesGene regulatory networkComputational biologyBiologyGenomeInteractomeGenetic divergence03 medical and health sciencesNetwork motif0302 clinical medicineGene duplicationDivergence (statistics)Gene030217 neurology & neurosurgery030304 developmental biologyProceedings of the Tenth International Conference on Computational Systems-Biology and Bioinformatics
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Network motif-based analysis of regulatory patterns in paralogous gene pairs

2020

Current high-throughput experimental techniques make it feasible to infer gene regulatory interactions at the whole-genome level with reasonably good accuracy. Such experimentally inferred regulatory networks have become available for a number of simpler model organisms such as S. cerevisiae, and others. The availability of such networks provides an opportunity to compare gene regulatory processes at the whole genome level, and in particular, to assess similarity of regulatory interactions for homologous gene pairs either from the same or from different species. We present here a new technique for analyzing the regulatory interaction neighborhoods of paralogous gene pairs. Our central focu…

0303 health sciencesGenomeGene regulatory networkComputational BiologyWhole genome duplicationSaccharomyces cerevisiaeComputational biologyParalogous GeneBiologyBiochemistryComputer Science ApplicationsEvolution Molecular03 medical and health sciencesNetwork motif0302 clinical medicineGene DuplicationEscherichia coliAnimalsGene Regulatory NetworksCaenorhabditis elegansMolecular BiologyGene030217 neurology & neurosurgeryTranscription Factors030304 developmental biologyJournal of Bioinformatics and Computational Biology
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Genetic alterations and oxidative metabolism in sporadic colorectal tumors from a Spanish community

1997

Deletions of loci on chromosomes 5q, 17p, 18q, and 22q, together with the incidence of p53 mutations and amplification of the double minute-2 gene were investigated in the sporadic colorectal tumors of 44 patients from a Spanish community. Chromosome deletions were analyzed by means of loss of heterozygosity analysis using a restriction fragment length polymorphism assay. Allelic losses were also detected by polymerase chain reaction (PCR)-single-stranded conformation polymorphism (SSCP) analysis of a polymorphic site in intron 2 of the p53 gene. The percentages of genetic deletions on the screened chromosomes were 39.3% (5q), 58.3% (17p), 40.9% (18q), and 40% (22q). Mutations in p53 exons …

AdultGenetic MarkersMaleGenome instabilityHeterozygoteLipid PeroxidesCancer ResearchChromosomes Human Pair 22DNA Mutational AnalysisAdenocarcinomaBiologymedicine.disease_causeLoss of heterozygosityProto-Oncogene ProteinsGene duplicationmedicineHumansMolecular BiologyGenePolymorphism Single-Stranded ConformationalAgedSequence DeletionGene AmplificationDeoxyguanosineNuclear ProteinsProto-Oncogene Proteins c-mdm2Single-strand conformation polymorphismDNA NeoplasmMiddle AgedGenes p53GlutathioneMolecular biology8-Hydroxy-2'-DeoxyguanosineChromosomes Human Pair 1SpainGenetic markerChromosomes Human Pair 5FemaleRestriction fragment length polymorphismChromosomes Human Pair 18Colorectal NeoplasmsCarcinogenesisOxidation-Reduction
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