Search results for "RNA Splicing"

showing 10 items of 109 documents

Stage, tissue, and cell specific distribution of alternative Ultrabithorax mRNAs and protein isoforms in the Drosophila embryo

1996

The homeotic gene Ultrabithorax encodes a family of six homeoproteins translated from alternatively spliced mRNAs. The structures of these UBX isoforms have been conserved among anciently diverged Drosoph-ila species and functional distinctions between some isoforms have been reported that suggest subtle but important roles in Ubx action. We present a detailed analysis of the expression patterns of Ubx mRNAs and proteins during embryogenesis, using isoform-specific monoclonal antibodies and synthetic oligonucleotide probes. These patterns are remarkably complex, each mRNA and corresponding protein isoform being expressed in a partially overlapping but distinct stage and tissue-specific patt…

GeneticsGene isoformProtein isoformMessenger RNAExonRNA splicingGeneticsIntronBiologyHomeotic geneUltrabithoraxDevelopmental BiologyRoux's Archives of Developmental Biology
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A chimeric ribozyme in Clostridium difficile combines features of group I introns and insertion elements

2002

CdlSt1, a DNA insertion of 1975 bp, was identified within tcdA-C34, the enterotoxin gene of the Clostridium difficile isolate C34. Located in the catalytic domain A1-C34, Cd/St1 combines features of two genetic elements. Within the first 434 nt structures characteristic for group I introns were found; encoding the two transposase-like proteins tlpA and tlpB nucleotides 435-1975 represent the remainder of a IS605-like insertion element. We show that the entire CdlSt1 is accurately spliced from tcdA-C34 primary transcripts and that purified TcdA-C34 toxin is of regular size and catalytic activity. A search for CdlSt1-related sequences demonstrates that the element is widespread in toxinogenic…

GeneticsOpen reading framebiologyRNA splicingIntronRibozymebiology.proteinInterrupted geneGroup I catalytic intronGroup II intronORFSMolecular BiologyMicrobiologyMolecular Microbiology
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Thirty-four novel mutations of the GLA gene in 121 patients with Fabry disease

2005

Fabry disease (FD) is an X-chromosomal disorder caused by mutations in the GLA gene encoding the lysosomal enzyme alpha-galactosidase A. We performed mutation screening on a cohort of 121 patients including 84 male and 37 female index cases and identified a total of 90 different mutations, 34 of which are reported for the first time here. Both point mutations (74.4%) and 'short length' rearrangements (25.6%) were found, including missense (54.4%), nonsense (14.4%), and splice site point mutations (5.6%), deletions (17.8%) or insertions/duplications (5.6%) of a few nucleotides, and complex rearrangements including larger deletions (2.2%). GLA mutations were identified in 82 (97.6%) of the 84…

GeneticsPoint mutationmedia_common.quotation_subjectNonsenseBiologymedicine.diseaseFabry diseaseGla geneRNA splicingGeneticsmedicineMutation screeningMissense mutationPeptide sequenceGenetics (clinical)media_commonHuman Mutation
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Demonstration that the Group II Intron from the Clostridial Conjugative Transposon Tn5397 Undergoes Splicing In Vivo

2001

Previous work has identified the conjugative transposon Tn5397 from Clostridium difficile. This element was shown to contain a group II intron. Tn5397 can be conjugatively transferred from C. difficile to Bacillus subtilis. In this work we show that the intron is spliced in both these hosts and that nonspliced RNA is also present. We constructed a mutation in the open reading frame within the intron, and this prevented splicing but did not prevent the formation of the circular form of the conjugative transposon (the likely transposition intermediate) or decrease the frequency of intergeneric transfer of Tn5397. Therefore, the intron is spliced, but splicing is not required for conjugation o…

GeneticsTransposable elementMutationClostridioides difficileRNA SplicingIntronRNAGroup II intronBiologymedicine.disease_causeMicrobiologyIntronsTransposition (music)Open reading frameRNA BacterialConjugation GeneticRNA splicingmedicineDNA Transposable ElementsRNA MessengerMolecular BiologyPlasmids and TransposonsBacillus subtilis
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Focal Transcriptional Activity of Murine Cytomegalovirus during Latency in the Lungs

1999

ABSTRACT Interstitial pneumonia is a frequent and critical manifestation of human cytomegalovirus (CMV) disease in immunocompromised patients, in particular in recipients of bone marrow transplantation. Previous work in the murine CMV infection model has identified the lungs as a major organ site of CMV latency and recurrence. It was open to question whether the viral genome is transcriptionally silent or active during latency. Transcription could be latency associated and thus be part of the latency phenotype. Alternatively, transcriptional activity could reflect episodes of reactivation. We demonstrate here that transcription of the immediate-early (IE) transcription unit ie1-ie3 selectiv…

Human cytomegalovirusMaleMuromegalovirusTranscription GeneticRNA SplicingImmunologyReplicationBiologyMicrobiologyTransactivationExonMiceMuromegalovirusTranscription (biology)Bone MarrowRecurrenceVirologyVirus latencyGene expressionmedicineAnimalsGeneGenes Immediate-EarlyLungExonsmedicine.diseasebiology.organism_classificationVirologyVirus LatencyInsect ScienceImmunologyDNA ViralFemale
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Intragenic FMR1 disease-causing variants: a significant mutational mechanism leading to Fragile-X syndrome

2017

International audience; Fragile-X syndrome (FXS) is a frequent genetic form of intellectual disability (ID). The main recurrent mutagenic mechanism causing FXS is the expansion of a CGG repeat sequence in the 5'-UTR of the FMR1 gene, therefore, routinely tested in ID patients. We report here three FMR1 intragenic pathogenic variants not affecting this sequence, identified using high-throughput sequencing (HTS): a previously reported hemizygous deletion encompassing the last exon of FMR1, too small to be detected by array-CGH and inducing decreased expression of a truncated form of FMRP protein, in three brothers with ID (family 1) and two splice variants in boys with sporadic ID: a de novo …

Male0301 basic medicinemedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesdiagnosisRNA SplicingBiologymedicine.disease_causePolymorphism Single NucleotideArticleFragile X Mental Retardation Protein03 medical and health sciencesExonGenetic linkageplacebo-controlled trial[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyMolecular geneticsGeneticsmedicineHumansgeneGenetics (clinical)GeneticsMutationintron 10SiblingsMiddle Agedmedicine.diseaseFMR1Human genetics3. Good healthFragile X syndromedevelopmental delayof-the-literature030104 developmental biologyintellectual disabilityFragile X SyndromeMutationmental-retardationMedical geneticsFemalepoint mutationdouble-blind[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Identification of Novel pro-α2(IX) Collagen Gene Mutations in Two Families with Distinctive Oligo-Epiphyseal Forms of Multiple Epiphyseal Dysplasia

1999

Multiple epiphyseal dysplasia (MED) is a genetically heterogeneous disorder with marked clinical and radiographic variability. Traditionally, the mild "Ribbing" and severe "Fairbank" types have been used to define a broad phenotypic spectrum. Mutations in the gene encoding cartilage oligomeric-matrix protein have been shown to result in several types of MED, whereas mutations in the gene encoding the alpha2 chain of type IX collagen (COL9A2) have so far been found only in two families with the Fairbank type of MED. Type IX collagen is a heterotrimer of pro-alpha chains derived from three distinct genes-COL9A1, COL9A2, and COL9A3. In this article, we describe two families with distinctive ol…

MaleAdolescentRNA SplicingMutantGene mutationBiologyOsteochondrodysplasiasmedicine.disease_causeMultiple epiphyseal dysplasia03 medical and health sciencesExon0302 clinical medicineOsteoarthritismedicineGeneticsHumansGenetics(clinical)Genetic TestingOsteochondrodysplasiaMultiple epiphyseal dysplasiaGene mutationAlleleChildPolymorphism Single-Stranded ConformationalGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesMutationType IX collagenGenetic heterogeneitymedicine.diseaseOsteochondrodysplasiaPedigreeRadiographyCartilageChild PreschoolMutationFemaleEpiphysesProcollagen030217 neurology & neurosurgeryResearch ArticleThe American Journal of Human Genetics
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Mutations in the mu heavy-chain gene in patients with agammaglobulinemia.

1996

Most patients with congenital hypogammaglobulinemia and absent B cells are males with X-linked agammaglobulinemia, which is caused by mutations in the gene for Bruton's tyrosine kinase (Btk); however, there are females with a similar disorder who do not have mutations in this gene. We studied two families with autosomal recessive defects in B-cell development and patients with presumed X-linked agammaglobulinemia who did not have mutations in Btk.A series of candidate genes that encode proteins involved in B-cell signal-transduction pathways were analyzed by linkage studies and mutation screening.Four different mutations were identified in the mu heavy-chain gene on chromosome 14. In one fa…

MaleCandidate geneGenetic LinkageDNA Mutational AnalysisConsanguinitymedicine.disease_causeConsanguinityGenetic linkageAgammaglobulinemiahemic and lymphatic diseasesmedicineBruton's tyrosine kinaseHumansLymphocyte CountGeneGeneticsChromosomes Human Pair 14MutationB-LymphocytesbiologyImmunoglobulin mu-ChainsChromosomeGeneral MedicinePedigreeRNA splicingMutationbiology.proteinFemaleThe New England journal of medicine
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Functional analysis of splicing mutations in MYO7A and USH2A genes.

2010

Usher syndrome is defined by the association of sensorineural hearing loss, retinitis pigmentosa and variable vestibular dysfunction. Many disease-causative mutations have been identified in MYO7A and USH2A genes, which play a major role in Usher syndrome type I and type II, respectively. The pathogenic nature of mutations that lead to premature stop codons is not questioned; nevertheless, additional studies are needed to verify the pathogenicity of some changes such as those putatively involved in the splice process. Five putative splice-site variants were detected in our cohort of patients: c.2283-1G>T and c.5856G>A in MYO7A and c.1841-2A>G, c.2167+5G>A and c.5298+1G>C in the USH2A gene. …

MaleGenotypeUsher syndromeRNA SplicingBiologyMyosinsmedicine.disease_causeExonChlorocebus aethiopsGene OrderGeneticsmedicineotorhinolaryngologic diseasesAnimalsHumansspliceGeneGenetics (clinical)GeneticsMutationExtracellular Matrix Proteinsmedicine.diseaseStop codonMyosin VIIaRNA splicingCOS CellsMutationFemaleRNA Splice SitesUsher SyndromesMinigeneClinical genetics
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Novel mutations of CETP gene in Italian subjects with hyeralphalipoproteinemia

2009

Abstract Cholesteryl ester transfer protein (CETP) is a plasma glycoprotein that catalyses the transfer of cholesteryl esters from HDL to the other plasma lipoproteins. Genetic deficiency of CETP is one of the known causes of elevation of plasma HDL-C (primary hyperalphalipoproteinemia, HALP). We sequenced CETP gene in a group of 24 Italian subjects with primary HALP (HDL-C>80 mg/dl) suspected to have CETP deficiency. Two unrelated subjects both coming from the same geographical district, were found to be heterozygous for a nucleotide substitution in exon 6 (c.544C>T) and another subject was found to be heterozygous for a C>T transition in exon 9 (c.802C>T). Both mutations introduce a prema…

MaleHyperlipoproteinemiasMessengerDNA Mutational Analysismedicine.disease_causeExonFamilial hyperalphalipoproteinemiaChlorocebus aethiopsCETP activity; CETP gene mutations; Familial hyperalphalipoproteinemia; HDL size; Adolescent; Adult; Aged; Animals; Biomarkers; COS Cells; Cercopithecus aethiops; Cholesterol Ester Transfer Proteins; Cholesterol HDL; DNA Mutational Analysis; European Continental Ancestry Group; Female; Humans; Hyperlipoproteinemias; Italy; Male; Middle Aged; Phenotype; RNA Messenger; Transfection; Up-Regulation; Young Adult; Mutation; Cardiology and Cardiovascular MedicineGeneticsMutationTransition (genetics)biologyCETP activityMiddle AgedUp-RegulationCholesterolPhenotypeItalyCOS CellsRNA splicingFemaleFamilial hyperalphalipoproteinemia; CETP gene mutations; CETP activity; HDL sizelipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineAdultHDLAdolescentEuropean Continental Ancestry GroupSocio-culturaleHDL sizeTransfectionWhite PeopleCercopithecus aethiopsYoung AdultCETP gene mutationsCholesterylester transfer proteinmedicineAnimalsHumansRNA MessengerGeneAgedCholesterol HDLIntroncetpCholesterol Ester Transfer Proteinscarbohydrates (lipids)biology.proteinRNAmutationBiomarkersMinigene
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