Search results for "MUTATION"

showing 10 items of 2830 documents

A glial amino-acid transporter controls synapse strength and courtship in Drosophila

2008

1097-6256 (Print) Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't; Mate choice is an evolutionarily critical decision that requires the detection of multiple sex-specific signals followed by central integration of these signals to direct appropriate behavior. The mechanisms controlling mate choice remain poorly understood. Here, we show that the glial amino-acid transporter genderblind controls whether Drosophila melanogaster males will attempt to mate with other males. Genderblind (gb) mutant males showed no alteration in heterosexual courtship or copulation, but were attracted to normally unappealing male species-specific chemosensory cues. As a resul…

Central Nervous SystemMaleNervous systemAmino Acid Transport System y+media_common.quotation_subjectNeuroscience(all)Glutamic AcidArticleAnimals Genetically ModifiedCourtshipSynapseGlutamatergicmedicineAnimalsDrosophila ProteinsRNA Small Interferingmedia_commonBehavior AnimalbiologyGeneral NeuroscienceCourtshipHomosexualitybiology.organism_classificationmedicine.anatomical_structureMate choiceMutationSynapsesGenderblindDrosophilaFemaleGlutamatergic synapseDrosophila melanogaster/dk/atira/pure/subjectarea/asjc/2800NeurogliaNeuroscience
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The commonly used marker ELAV is transiently expressed in neuroblasts and glial cells in theDrosophilaembryonic CNS

2007

Glial cells in the Drosophila embryonic nervous system can be monitored with the marker Reversed-polarity (Repo), whereas neurons lack Repo and express the RNA-binding protein ELAV (Embryonic Lethal, Abnormal Vision). Since the first description of the ELAV protein distribution in 1991 (Robinow and White), it is believed that ELAV is an exclusive neuronal and postmitotic marker. Looking at ELAV expression, we unexpectedly observed that, in addition to neurons, ELAV is transiently expressed in embryonic glial cells. Furthermore, it is transiently present in the proliferating longitudinal glioblast, and it is transcribed in embryonic neuroblasts. Likewise, elav-Gal4 lines, which are generally…

Central Nervous SystemNervous systemGenes InsectBiologyAnimals Genetically ModifiedGlioblastNeuroblastGenes ReportermedicineAnimalsDrosophila ProteinsEmbryonic Stem CellsNeuronsRegulation of gene expressionGene Expression Regulation DevelopmentalEmbryoAnatomyEmbryonic stem cellPhenotypeNeural stem cellCell biologyPhenotypemedicine.anatomical_structureELAV Proteinsnervous systemMutationDrosophilaNeurogliaDevelopmental BiologyDevelopmental Dynamics
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Programmed cell death in the embryonic central nervous system of Drosophila melanogaster.

2006

Although programmed cell death (PCD) plays a crucial role throughout Drosophila CNS development, its pattern and incidence remain largely uninvestigated. We provide here a detailed analysis of the occurrence of PCD in the embryonic ventral nerve cord (VNC). We traced the spatio-temporal pattern of PCD and compared the appearance of, and total cell numbers in,thoracic and abdominal neuromeres of wild-type and PCD-deficient H99mutant embryos. Furthermore, we have examined the clonal origin and fate of superfluous cells in H99 mutants by DiI labeling almost all neuroblasts, with special attention to segment-specific differences within the individually identified neuroblast lineages. Our data r…

Central Nervous SystemProgrammed cell deathanimal structuresEmbryo NonmammalianApoptosisCell CountBiologyNeuroblastInterneuronsmedicineAnimalsCell LineageMolecular BiologyBody PatterningNeuronsGene Expression Regulation DevelopmentalAnatomyNeuromerebiology.organism_classificationEmbryonic stem cellImmunohistochemistryCell biologyClone Cellsmedicine.anatomical_structureDrosophila melanogasternervous systemVentral nerve cordMutationNeuronDrosophila melanogasterGanglion mother cellDevelopmental BiologyDevelopment (Cambridge, England)
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The muscleblind gene participates in the organization of Z-bands and epidermal attachments of Drosophila muscles and is regulated by Dmef2.

1998

We report the embryonic phenotype of muscleblind (mbl), a recently described Drosophila gene involved in terminal differentiation of adult ommatidia. mbl is a nuclear protein expressed late in the embryo in pharyngeal, visceral, and somatic muscles, the ventral nerve cord, and the larval photoreceptor system. All three mbl alleles studied exhibit a lethal phenotype and die as stage 17 embryos or first instar larvae. These larvae are partially paralyzed, show a characteristically contracted abdomen, and lack striation of muscles. Our analysis of the somatic musculature shows that the pattern of muscles is established correctly, and they form morphologically normal synapses. Ultrastructural a…

Central Nervous SystemSomatic cellMuscle Fibers SkeletalNeuromuscular JunctionMuscle ProteinsGenes InsectBiologymuscle attachmentsmuscleblindMesodermTendonsEctodermAnimalsDrosophila ProteinsConnectinRNA MessengerNuclear proteinMuscle SkeletalMolecular BiologyZ-bandsCell NucleusEpidermis (botany)MyogenesisMEF2 Transcription FactorsDrosophila.Gene Expression Regulation DevelopmentalNuclear ProteinsEmbryoCell DifferentiationCell BiologyAnatomybacterial infections and mycosesEmbryonic stem cellPhenotypeCell biologyDNA-Binding ProteinsMyogenic Regulatory FactorsVentral nerve cordMutationInsect ProteinsDrosophilaPhotoreceptor Cells InvertebratemyogenesisDevelopmental BiologyTranscription FactorsDevelopmental biology
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Exacerbated experimental autoimmune encephalomyelitis in mast-cell-deficient KitW-sh/W-sh mice

2011

Mast cell (MC)-deficient c-Kit mutant Kit(W/W-v) mice are protected against experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, suggesting a detrimental role for MCs in this disease. To further investigate the role of MCs in EAE, we took advantage of a recently characterized model of MC deficiency, Kit(W-sh/W-sh). Surprisingly, we observed that myelin oligodendrocyte glycoprotein (MOG)(35-55)-induced chronic EAE was exacerbated in Kit(W-sh/W-sh) compared with Kit(+/+) mice. Kit(W-sh/W-sh) mice showed more inflammatory foci in the central nervous system (CNS) and increased T-cell response against myelin. To understand whether the discrepant results obtaine…

Central Nervous SystemT-LymphocytesEncephalomyelitisexperimental autoimmune encephalomyelitismast cellsInbred C57BLSeverity of Illness IndeximmunologyMiceMyelinPeptide Fragmentimmune system diseasesMast CellEncephalomyelitisMyelin SheathbiologyExperimental autoimmune encephalomyelitisMast cellProto-Oncogene Proteins c-kitPhenotypemedicine.anatomical_structuremastcell-deficient miceBone Marrow Cellgenetics/immunology/pathology/prevention /&/ controlc-kit mutationsc-kit mutations; experimental autoimmune encephalomyelitis; granulocytes; mast cellsEncephalomyelitis Autoimmune ExperimentalCentral nervous systemBone Marrow CellsPathology and Forensic MedicineMyelin oligodendrocyte glycoproteinExperimentalAnimals Antibody Formation Bone Marrow Cells; pathology Central Nervous System; pathology Encephalomyelitis; Autoimmune; Experimental; genetics/immunology/pathology/prevention /&/ control Glycoproteins; immunology Granulocytes; pathology Immunization Mast Cells; pathology Mice Mice; Inbred C57BL Mutation Myelin Sheath; immunology Myelin-Oligodendrocyte Glycoprotein Peptide Fragments; immunology Phenotype Proto-Oncogene Proteins c-kit; deficiency/genetics/metabolism Severity of Illness Index T-Lymphocytes; pathologyAntigendeficiency/genetics/metabolismmedicineAnimalsMolecular BiologyGlycoproteinsAnimalMultiple sclerosismast-cell-deficient Kit W-sh/W-sh mice.Experimental autoimmune encephalomyelitis; mast-cell-deficient Kit W-sh/W-sh mice.GranulocytegranulocytesCell Biologymedicine.diseaseEncephalomyelitiExperimental autoimmune encephalomyelitiPeptide FragmentsMice Inbred C57BLT-LymphocyteAntibody FormationMutationImmunologybiology.proteinexperimental autoimmune encephalomyelitis; mastcell-deficient mice; mast cellspathologyImmunizationMyelin-Oligodendrocyte GlycoproteinGlycoproteinAutoimmuneLaboratory Investigation
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Commitment of CNS Progenitors Along the Dorsoventral Axis of Drosophila Neuroectoderm

1995

In the Drosophila embryo, the central nervous system (CNS) develops from a population of neural stem cells (neuroblasts) and midline progenitor cells. Here, the fate and extent of determination of CNS progenitors along the dorsoventral axis was assayed. Dorsal neuroectodermal cells transplanted into the ventral neuroectoderm or into the midline produced CNS lineages consistent with their new position. However, ventral neuroectodermal cells and midline cells transplanted to dorsal sites of the neuroectoderm migrated ventrally and produced CNS lineages consistent with their origin. Thus, inductive signals at the ventral midline and adjacent neuroectoderm may confer ventral identities to CNS p…

Central Nervous SystemTransplantation Heterotopicanimal structuresCell TransplantationCentral nervous systemPopulationEctodermBiologyNeuroblastCell MovementEctodermmedicineAnimalsProgenitor celleducationNeuronseducation.field_of_studyMultidisciplinaryNeuroectodermStem CellsGastrulaAnatomyNeural stem cellCell biologyTransplantationmedicine.anatomical_structureMutationembryonic structuresDrosophilaNeurogliaStem Cell TransplantationScience
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Differential effects of EGF receptor signalling on neuroblast lineages along the dorsoventral axis of the Drosophila CNS

1998

ABSTRACT The Drosophila ventral nerve cord derives from a stereotype population of about 30 neural stem cells, the neuroblasts, per hemineuromere. Previous experiments provided indications for inductive signals at ventral sites of the neuroectoderm that confer neuroblast identities. Using cell lineage analysis, molecular markers and cell transplantation, we show here that EGF receptor signalling plays an instructive role in CNS patterning and exerts differential effects on dorsoventral subpopulations of neuroblasts. The Drosophila EGF receptor (DER) is capable of cell autonomously specifiying medial and intermediate neuroblast cell fates. DER signalling appears to be most critical for prope…

Central Nervous Systemanimal structuresPopulationCell fate determinationBiologyNeuroblastEctodermAnimalseducationReceptorMolecular BiologyBody PatterningNeuronseducation.field_of_studyNeuroectodermStem CellsfungiAnatomyNeural stem cellCell biologyErbB Receptorsnervous systemVentral nerve cordMutationembryonic structuresDrosophilaGanglion mother cellBiomarkersSignal TransductionStem Cell TransplantationDevelopmental BiologyDevelopment
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CNS involvement in OFD1 syndrome: a clinical, molecular, and neuroimaging study

2014

Background Oral-facial-digital type 1 syndrome (OFD1; OMIM 311200) belongs to the expanding group of disorders ascribed to ciliary dysfunction. With the aim of contributing to the understanding of the role of primary cilia in the central nervous system (CNS), we performed a thorough characterization of CNS involvement observed in this disorder. Methods A cohort of 117 molecularly diagnosed OFD type I patients was screened for the presence of neurological symptoms and/or cognitive/behavioral abnormalities on the basis of the available information supplied by the collaborating clinicians. Seventy-one cases showing CNS involvement were further investigated through neuroimaging studies and neur…

Central nervous systemNeuroimagingNeuropsychological TestsPharmacologyBioinformaticsSettore MED/03 - GENETICA MEDICACiliopathiesCohort Studies03 medical and health sciences0302 clinical medicineNeuroimagingCentral Nervous System DiseasesmedicineHumansGenetics(clinical)Pharmacology (medical)Orofaciodigital type 1Ciliopathies; Neurodevelopmental phenotype; Neuroimaging; OFD1; Central Nervous System Diseases; Cohort Studies; Female; Humans; Magnetic Resonance Imaging; Mutation; Neuropsychological Tests; Orofaciodigital Syndromes; Medicine (all); Genetics (clinical); Pharmacology (medical)Agenesis of the corpus callosumGenetics (clinical)030304 developmental biologyMedicine(all)0303 health sciencesbusiness.industryMedicine (all)ResearchCiliumNeuropsychologyCognitionGeneral MedicineOrofaciodigital Syndromesmedicine.diseasecentral nervous systemMagnetic Resonance ImagingPorencephalyCiliopathies3. Good healthmedicine.anatomical_structureMutationFemaleNeurodevelopmental phenotypeOFD1business030217 neurology & neurosurgeryOrphanet Journal of Rare Diseases
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RPGR ORF15 isoform co-localizes with RPGRIP1 at centrioles and basal bodies and interacts with nucleophosmin

2005

The ORF15 isoform of RPGR (RPGR(ORF15)) and RPGR interacting protein 1 (RPGRIP1) are mutated in a variety of retinal dystrophies but their functions are poorly understood. Here, we show that in cultured mammalian cells both RPGR(ORF15) and RPGRIP1 localize to centrioles. These localizations are resistant to the microtubule destabilizing drug nocodazole and persist throughout the cell cycle. RPGR and RPGRIP1 also co-localize at basal bodies in cells with primary cilia. The C-terminal (C2) domain of RPGR(ORF15) (ORF15(C2)) is highly conserved across 13 mammalian species, suggesting that it is a functionally important domain. Using matrix-assisted laser desorption ionization time-of-flight mas…

CentrioleFluorescent Antibody TechniqueMicechemistry.chemical_compoundChlorocebus aethiopsGuanine Nucleotide Exchange FactorsProtein IsoformsBasal bodyConserved SequenceGenetics (clinical)CentriolesGlutathione Transferaseintegumentary systemNuclear ProteinsExonsGeneral MedicineRetinitis pigmentosa GTPase regulatorImmunohistochemistryNocodazoleCOS CellsNucleophosminCell NucleolusRecombinant Fusion ProteinsMolecular Sequence DataBiologyOpen Reading FramesMicrotubuleTwo-Hybrid System TechniquesGeneticsAnimalsHumansAmino Acid SequenceEye ProteinsMolecular BiologyNucleophosminSequence Homology Amino AcidProteinsPrecipitin TestsMolecular biologyeye diseasesProtein Structure TertiaryMice Inbred C57BLCytoskeletal ProteinschemistryCentrosomeCytoplasmSpectrometry Mass Matrix-Assisted Laser Desorption-IonizationMutationCattleHeLa CellsHuman Molecular Genetics
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The retinitis pigmentosa 28 protein FAM161A is a novel ciliary protein involved in intermolecular protein interaction and microtubule association

2012

Loss-of-function mutations in the gene encoding FAM161A were recently discovered as the cause for RP28, an autosomal recessive form of retinitis pigmentosa. To initiate the characterization of the cellular role of FAM161A in the retina, we focused on its subcellular localization and conducted in vitro studies to identify FAM161A-interacting proteins and associated cellular structures. Immunohistochemistry revealed the presence of mouse FAM161A in the photoreceptor inner segments, the synaptic regions of the outer and inner plexiform layers and the ganglion cells. In mouse and human retinal sections from unfixed eyes, FAM161A localized to the ciliary region linking photoreceptor outer and in…

CentrioleImmunoelectron microscopyBiologyMicrotubulesRetinaMice03 medical and health sciences0302 clinical medicineMicrotubuleRetinitis pigmentosaGeneticsmedicineAnimalsHumansBasal bodyPhotoreceptor CellsEye ProteinsMolecular BiologyGenetics (clinical)030304 developmental biologyCentrosome0303 health sciencesRetinaCiliumGeneral Medicinemedicine.diseaseCell biologymedicine.anatomical_structureCentrosomeMutationsense organsRetinitis Pigmentosa030217 neurology & neurosurgeryHuman Molecular Genetics
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