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  1 / 1794 MEDLINE  
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[PMID]:29366779
[Au] Autor:Fukumura K; Inoue K; Mayeda A
[Ad] Endereço:Division of Gene Expression Mechanism, Institute for Comprehensive Medical Science, Fujita Health University, Toyoake 470-1192, Aichi, Japan.
[Ti] Título:Splicing activator RNPS1 suppresses errors in pre-mRNA splicing: A key factor for mRNA quality control.
[So] Source:Biochem Biophys Res Commun;496(3):921-926, 2018 02 12.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human RNPS1 protein was first identified as a pre-mRNA splicing activator in vitro and RNPS1 regulates alternative splicing in cellulo. RNPS1 was also known as a peripheral factor of the exon junction complex (EJC). Here we show that cellular knockdown of RNPS1 induced a reduction of the wild-type aurora kinase B (AURKB) protein due to the induced aberrant pre-mRNA splicing events, indicating that the fidelity of AURKB pre-mRNA splicing was reduced. The major aberrant AURKB mRNA was derived from the upstream pseudo 5' and 3' splice sites in intron 5, which resulted in the production of the non-functional truncated AURKB protein. AURKB, is an essential mitotic factor, whose absence is known to cause multiple nuclei, and this multinucleation phenotype was recapitulated in RNPS1-knockdown cells. Importantly this RNPS1-knockdown phenotype was rescued by ectopic expression of AURKB, implying it is a major functional target of RNPS1. We found RNPS1 protein, not as a component of the EJC, binds directly to a specific element in the AURKB exon upstream of the authentic 5' splice site, and this binding is required for normal splicing. RNPS1-knockdown induces a parallel aberrant splicing pattern in a fully distinct pre-mRNA, MDM2, suggesting that RNPS1 is a global guardian of splicing fidelity. We conclude that RNPS1 is a key factor for the quality control of mRNAs that is essential for the phenotypes including cell division.
[Mh] Termos MeSH primário: Aurora Quinase B/genética
Genes Supressores
Precursores de RNA/genética
Processamento de RNA/genética
RNA Mensageiro/genética
Ribonucleoproteínas/genética
[Mh] Termos MeSH secundário: Células HeLa
Seres Humanos
Controle de Qualidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (RNA Precursors); 0 (RNA, Messenger); 0 (RNPS1 protein, human); 0 (Ribonucleoproteins); EC 2.7.11.1 (AURKB protein, human); EC 2.7.11.1 (Aurora Kinase B)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE


  2 / 1794 MEDLINE  
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[PMID]:28803967
[Au] Autor:Wang W; Perens EA; Oikonomou G; Wallace SW; Lu Y; Shaham S
[Ad] Endereço:Laboratory of Developmental Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
[Ti] Título:IGDB-2, an Ig/FNIII protein, binds the ion channel LGC-34 and controls sensory compartment morphogenesis in C. elegans.
[So] Source:Dev Biol;430(1):105-112, 2017 10 01.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sensory organ glia surround neuronal receptive endings (NREs), forming a specialized compartment important for neuronal activity, and reminiscent of glia-ensheathed synapses in the central nervous system. We previously showed that DAF-6, a Patched-related protein, is required in glia of the C. elegans amphid sensory organ to restrict sensory compartment size. LIT-1, a Nemo-like kinase, and SNX-1, a retromer component, antagonize DAF-6 and promote compartment expansion. To further explore the machinery underlying compartment size control, we sought genes whose inactivation restores normal compartment size to daf-6 mutants. We found that mutations in igdb-2, encoding a single-pass transmembrane protein containing Ig-like and fibronectin type III domains, suppress daf-6 mutant defects. IGDB-2 acts in glia, where it localizes to glial membranes surrounding NREs, and, together with LIT-1 and SNX-1, regulates compartment morphogenesis. Immunoprecipitation followed by mass spectrometry demonstrates that IGDB-2 binds to LGC-34, a predicted ligand-gated ion channel, and lgc-34 mutations inhibit igdb-2 suppression of daf-6. Our findings reveal a novel membrane protein complex and suggest possible mechanisms for how sensory compartment size is controlled.
[Mh] Termos MeSH primário: Proteínas de Caenorhabditis elegans/metabolismo
Caenorhabditis elegans/metabolismo
Compartimento Celular
Morfogênese
Células Receptoras Sensoriais/citologia
Células Receptoras Sensoriais/metabolismo
[Mh] Termos MeSH secundário: Alelos
Animais
Caenorhabditis elegans/genética
Proteínas de Caenorhabditis elegans/química
Proteínas de Caenorhabditis elegans/genética
Membrana Celular/metabolismo
Epistasia Genética
Genes Supressores
Células HEK293
Seres Humanos
Ligantes
Modelos Biológicos
Mutação/genética
Neuroglia/metabolismo
Ligação Proteica
Domínios Proteicos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Caenorhabditis elegans Proteins); 0 (Ligands)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170815
[St] Status:MEDLINE


  3 / 1794 MEDLINE  
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[PMID]:28526948
[Au] Autor:Rodríguez-García ME; Cotrina-Vinagre FJ; Carnicero-Rodríguez P; Martínez-Azorín F
[Ad] Endereço:Laboratorio de Enfermedades Mitocondriales, Instituto de Investigación Hospital 12 de Octubre (i+12), Centro de Actividades Ambulatorias (CAA), 6a Planta, Bloque E, Avda. Córdoba s/n, 28041, Madrid, Spain.
[Ti] Título:An innovative strategy to clone positive modifier genes of defects caused by mtDNA mutations: MRPS18C as suppressor gene of m.3946G>A mutation in MT-ND1 gene.
[So] Source:Hum Genet;136(7):885-896, 2017 Jul.
[Is] ISSN:1432-1203
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:We have developed a new functional complementation approach to clone modifier genes which overexpression is able to suppress the biochemical defects caused by mtDNA mutations (suppressor genes). This strategy consists in transferring human genes into respiratory chain-deficient fibroblasts, followed by a metabolic selection in a highly selective medium. We used a normalized expression cDNA library in an episomal vector (pREP4) to transfect the fibroblasts, and a medium with glutamine and devoid of any carbohydrate source to select metabolically. Growing the patient's fibroblasts in this selective medium, the deficient cells rapidly disappear unless they are rescued by the cDNA of a suppressor gene. The use of an episomal vector allows us to carry out several rounds of transfection/selection (cyclical phenotypic rescue) to enrich the rescue with true clones of suppressor genes. Using fibroblasts from a patient with epileptic encephalopathy with the m.3946G>A (p.E214K) mutation in the MT-ND1 gene, several candidate genes were identified and one of them was characterized functionally. Thus, overexpression of MRPS18C gene (that encode for bS18m protein) suppressed the molecular defects produced by this mtDNA mutation, recovering the complex I activity and reducing the ROS produced by this complex to normal levels. We suggest that modulation of bS18m expression may be an effective therapeutic strategy for the patients with this mutation.
[Mh] Termos MeSH primário: DNA Mitocondrial/genética
Genes Modificadores
Genes Supressores
Proteínas Mitocondriais/genética
Proteínas Ribossômicas/genética
[Mh] Termos MeSH secundário: Células Cultivadas
Fibroblastos/citologia
Fibroblastos/metabolismo
Regulação da Expressão Gênica
Biblioteca Gênica
Seres Humanos
Mutação
NADH Desidrogenase/genética
RNA Longo não Codificante/genética
RNA Longo não Codificante/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Análise de Sequência de DNA
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Mitochondrial); 0 (MRPS18C protein, human); 0 (Mitochondrial Proteins); 0 (RNA, Long Noncoding); 0 (Reactive Oxygen Species); 0 (Ribosomal Proteins); EC 1.6.99.3 (NADH Dehydrogenase); EC 1.6.99.3 (NADH dehydrogenase subunit 1, human)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170521
[St] Status:MEDLINE
[do] DOI:10.1007/s00439-017-1812-9


  4 / 1794 MEDLINE  
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[PMID]:28356157
[Au] Autor:Srinivasainagendra V; Sandel MW; Singh B; Sundaresan A; Mooga VP; Bajpai P; Tiwari HK; Singh KK
[Ad] Endereço:Department of Biostatistics, School of Public Health, University of Alabama at Birmingham, Birmingham, Alabama, 35294, USA.
[Ti] Título:Migration of mitochondrial DNA in the nuclear genome of colorectal adenocarcinoma.
[So] Source:Genome Med;9(1):31, 2017 Mar 29.
[Is] ISSN:1756-994X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Colorectal adenocarcinomas are characterized by abnormal mitochondrial DNA (mtDNA) copy number and genomic instability, but a molecular interaction between mitochondrial and nuclear genome remains unknown. Here we report the discovery of increased copies of nuclear mtDNA (NUMT) in colorectal adenocarcinomas, which supports link between mtDNA and genomic instability in the nucleus. We name this phenomenon of nuclear occurrence of mitochondrial component as numtogenesis. We provide a description of NUMT abundance and distribution in tumor versus matched blood-derived normal genomes. METHODS: Whole-genome sequence data were obtained for colon adenocarcinoma and rectum adenocarcinoma patients participating in The Cancer Genome Atlas, via the Cancer Genomics Hub, using the GeneTorrent file acquisition tool. Data were analyzed to determine NUMT proportion and distribution on a genome-wide scale. A NUMT suppressor gene was identified by comparing numtogenesis in other organisms. RESULTS: Our study reveals that colorectal adenocarcinoma genomes, on average, contains up to 4.2-fold more somatic NUMTs than matched normal genomes. Women colorectal tumors contained more NUMT than men. NUMT abundance in tumor predicted parallel abundance in blood. NUMT abundance positively correlated with GC content and gene density. Increased numtogenesis was observed with higher mortality. We identified YME1L1, a human homolog of yeast YME1 (yeast mitochondrial DNA escape 1) to be frequently mutated in colorectal tumors. YME1L1 was also mutated in tumors derived from other tissues. We show that inactivation of YME1L1 results in increased transfer of mtDNA in the nuclear genome. CONCLUSIONS: Our study demonstrates increased somatic transfer of mtDNA in colorectal tumors. Our study also reveals sex-based differences in frequency of NUMT occurrence and that NUMT in blood reflects NUMT in tumors, suggesting NUMT may be used as a biomarker for tumorigenesis. We identify YME1L1 as the first NUMT suppressor gene in human and demonstrate that inactivation of YME1L1 induces migration of mtDNA to the nuclear genome. Our study reveals that numtogenesis plays an important role in the development of cancer.
[Mh] Termos MeSH primário: Adenocarcinoma/genética
Núcleo Celular/metabolismo
Neoplasias Colorretais/genética
DNA Mitocondrial
Genoma
Metaloendopeptidases/genética
[Mh] Termos MeSH secundário: ATPases Associadas a Diversas Atividades Celulares
Adenocarcinoma/etiologia
Adenocarcinoma/metabolismo
Adenocarcinoma/mortalidade
Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Criança
Pré-Escolar
Neoplasias Colorretais/etiologia
Neoplasias Colorretais/metabolismo
Neoplasias Colorretais/mortalidade
DNA de Neoplasias
Feminino
Genes Supressores
Genoma Humano
Genoma Mitocondrial
Genômica
Seres Humanos
Lactente
Recém-Nascido
Masculino
Meia-Idade
Proteínas Mitocondriais
Mutação
Fatores Sexuais
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Mitochondrial); 0 (DNA, Neoplasm); 0 (Mitochondrial Proteins); EC 3.4.24.- (Metalloendopeptidases); EC 3.4.24.- (YME1L1 protein, human); EC 3.6.4.- (ATPases Associated with Diverse Cellular Activities)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170331
[St] Status:MEDLINE
[do] DOI:10.1186/s13073-017-0420-6


  5 / 1794 MEDLINE  
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[PMID]:28089773
[Au] Autor:Francisci S; Montanari A
[Ad] Endereço:Department of Biology and Biotechnologies "Charles Darwin", Sapienza University of Rome, Piazzale Aldo Moro, 5, 00185 Rome, Italy. Electronic address: silvia.francisci@uniroma1.it.
[Ti] Título:Mitochondrial diseases: Yeast as a model for the study of suppressors.
[So] Source:Biochim Biophys Acta;1864(4):666-673, 2017 04.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Mitochondrial (mt) tRNA gene mutations are an important cause of human morbidity and are associated with different syndromes. We have previously shown that the mitochondrial protein synthesis elongation factor EF-Tu and isolated sequences from the carboxy-terminal domain of yeast and human mt leucyl-tRNA synthetases (LeuRS), have a wide range of suppression capability among different yeast mt tRNA mutants having defective respiratory phenotype. Here we show that the rescuing capability can be restricted to a specific sequence of six amino acids from the carboxy-terminal domain of mt LeuRS. On the other hand by overexpressing a mutated version of mt EF-Tu in a yeast strain deleted for the endogenous nuclear gene we identified the specific region involved in suppression. Results support the possibility that a small peptide could correct defects associated with many mt tRNA mutations, suggesting a novel therapy for mitochondrial diseases treatment. The involvement of the mt EF-Tu in cellular heat stress response has also been suggested.
[Mh] Termos MeSH primário: Regulação Fúngica da Expressão Gênica
Leucina-tRNA Ligase/genética
Mitocôndrias/genética
Proteínas Mitocondriais/genética
Fator Tu de Elongação de Peptídeos/genética
RNA de Transferência/genética
Saccharomyces cerevisiae/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Genes Supressores
Teste de Complementação Genética
Temperatura Alta
Seres Humanos
Leucina-tRNA Ligase/metabolismo
Mitocôndrias/metabolismo
Mitocôndrias/patologia
Doenças Mitocondriais/genética
Doenças Mitocondriais/metabolismo
Doenças Mitocondriais/patologia
Proteínas Mitocondriais/metabolismo
Modelos Biológicos
Mutação
Fator Tu de Elongação de Peptídeos/metabolismo
RNA/genética
RNA/metabolismo
RNA de Transferência/metabolismo
Saccharomyces cerevisiae/metabolismo
Estresse Fisiológico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Mitochondrial Proteins); 0 (RNA, mitochondrial); 63231-63-0 (RNA); 9014-25-9 (RNA, Transfer); EC 3.6.1.- (Peptide Elongation Factor Tu); EC 6.1.1.4 (Leucine-tRNA Ligase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170117
[St] Status:MEDLINE


  6 / 1794 MEDLINE  
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[PMID]:28057300
[Au] Autor:Krench M; Littleton JT
[Ad] Endereço:The Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, United States.
[Ti] Título:Neurotoxicity Pathways in Drosophila Models of the Polyglutamine Disorders.
[So] Source:Curr Top Dev Biol;121:201-223, 2017.
[Is] ISSN:1557-8933
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although polyglutamine expansion diseases are the most common genetically inherited neurodegenerative disorders, the key pathogenic mechanisms that lead to neuronal cell death are unclear. The expansion of a polyglutamine tract in specific proteins is the defining molecular insult, leading to cell-type and region-specific neuronal death. Intraneuronal aggregates of the affected protein can be found in the nucleus and/or cytoplasm and are a hallmark of these disorders. Whether and how aggregation leads to pathology, however, is under debate. In this chapter, we will review some of the key observations using Drosophila models of polyglutamine disorders that have highlighted a host of potential contributing pathologies, including defects in transcription, autophagy, and mitochondrial biology. We will also examine how genetic screening approaches have been used in Drosophila to provide insights into potential therapeutic approaches for polyglutamine disorders.
[Mh] Termos MeSH primário: Modelos Animais de Doenças
Drosophila/fisiologia
Doenças Neurodegenerativas/patologia
Neurotoxinas/toxicidade
Peptídeos/metabolismo
[Mh] Termos MeSH secundário: Animais
Autofagia
Drosophila/genética
Genes Supressores
Seres Humanos
Doenças Neurodegenerativas/genética
Peptídeos/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Neurotoxins); 0 (Peptides); 26700-71-0 (polyglutamine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170508
[Lr] Data última revisão:
170508
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170107
[St] Status:MEDLINE


  7 / 1794 MEDLINE  
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[PMID]:28049717
[Au] Autor:Pergolizzi B; Bracco E; Bozzaro S
[Ad] Endereço:Department of Clinical and Biological Sciences, University of Torino, AOU S. Luigi, Orbassano (TO) 10043, Italy.
[Ti] Título:A new HECT ubiquitin ligase regulating chemotaxis and development in Dictyostelium discoideum.
[So] Source:J Cell Sci;130(3):551-562, 2017 Feb 01.
[Is] ISSN:1477-9137
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cyclic AMP (cAMP) binding to G-protein-coupled receptors (GPCRs) orchestrates chemotaxis and development in Dictyostelium. By activating the RasC-TORC2-PKB (PKB is also known as AKT in mammals) module, cAMP regulates cell polarization during chemotaxis. TORC2 also mediates GPCR-dependent stimulation of adenylyl cyclase A (ACA), enhancing cAMP relay and developmental gene expression. Thus, mutants defective in the TORC2 Pia subunit (also known as Rictor in mammals) are impaired in chemotaxis and development. Near-saturation mutagenesis of a Pia mutant by random gene disruption led to selection of two suppressor mutants in which spontaneous chemotaxis and development were restored. PKB phosphorylation and chemotactic cell polarization were rescued, whereas Pia-dependent ACA stimulation was not restored but bypassed, leading to cAMP-dependent developmental gene expression. Knocking out the gene encoding the adenylylcyclase B (ACB) in the parental strain showed ACB to be essential for this process. The gene tagged in the suppressor mutants encodes a newly unidentified HECT ubiquitin ligase that is homologous to mammalian HERC1, but harbours a pleckstrin homology domain. Expression of the isolated wild-type HECT domain, but not a mutant HECT C5185S form, from this protein was sufficient to reconstitute the parental phenotype. The new ubiquitin ligase appears to regulate cell sensitivity to cAMP signalling and TORC2-dependent PKB phosphorylation.
[Mh] Termos MeSH primário: Quimiotaxia
Dictyostelium/citologia
Dictyostelium/enzimologia
Proteínas de Protozoários/metabolismo
Ubiquitina-Proteína Ligases/metabolismo
[Mh] Termos MeSH secundário: Adenilil Ciclases/metabolismo
Polaridade Celular
AMP Cíclico/metabolismo
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
DNA/metabolismo
Dictyostelium/genética
Proteínas de Ligação ao GTP/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Genes Supressores
Modelos Biológicos
Mutação/genética
Fenótipo
Fosforilação
Domínios Proteicos
Proteínas de Protozoários/química
Transdução de Sinais
Especificidade por Substrato
Ubiquitina-Proteína Ligases/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protozoan Proteins); 9007-49-2 (DNA); E0399OZS9N (Cyclic AMP); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 3.6.1.- (GTP-Binding Proteins); EC 4.6.1.1 (Adenylyl Cyclases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170804
[Lr] Data última revisão:
170804
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170105
[St] Status:MEDLINE
[do] DOI:10.1242/jcs.194225


  8 / 1794 MEDLINE  
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[PMID]:28007972
[Au] Autor:Hou J; Schacherer J
[Ad] Endereço:Department of Genetics, Genomics and Microbiology, University of Strasbourg, Strasbourg, France.
[Ti] Título:Fitness Trade-Offs Lead to Suppressor Tolerance in Yeast.
[So] Source:Mol Biol Evol;34(1):110-118, 2017 Jan.
[Is] ISSN:1537-1719
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Genetic variation among individuals within a population provides the raw material for phenotypic diversity upon which natural selection operates. Some given variants can act on multiple standing genomic variations simultaneously and release previously inaccessible phenotypes, leading to increased adaptive potential upon challenging environments. Previously, we identified such a variant related to a tRNA nonsense suppressor in yeast. When introduced into other genetic backgrounds, the suppressor led to an increased population phenotypic variance on various culture conditions, conferring background and environment specific selective advantages. Nonetheless, most isolates are intolerant to the suppressor on rich media due to a severe fitness cost. Here, we found that the tolerance to suppressor is related to a surprising level of fitness outburst, showing a trade-off effect to accommodate the cost of carrying the suppressor. To dissect the genetic basis of such trade-offs, we crossed strains with contrasting tolerance levels on rich media, and analyzed the fitness distribution patterns in the offspring. Combining quantitative tetrad analysis and bulk segregant analysis, we identified two genes, namely MKT1 and RGA1, involved in suppressor tolerance. We showed that alleles from the tolerant parent for both genes conferred a significant gain of fitness, which increased the suppressor tolerance. Our results present a detailed dissection of suppressor tolerance in yeast and provide insights into the molecular basis of trade-offs between fitness and evolutionary potential.
[Mh] Termos MeSH primário: Aptidão Genética
Saccharomyces cerevisiae/genética
[Mh] Termos MeSH secundário: Adaptação Fisiológica/genética
Alelos
Evolução Biológica
Genes Supressores
Variação Genética
Locos de Características Quantitativas
Seleção Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161224
[St] Status:MEDLINE
[do] DOI:10.1093/molbev/msw225


  9 / 1794 MEDLINE  
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[PMID]:27974497
[Au] Autor:Cole AE; Hani FM; Altman R; Meservy M; Roth JR; Altman E
[Ad] Endereço:Department of Biology, Middle Tennessee State University, Murfreesboro, Tennessee 37132.
[Ti] Título:The Promiscuous sumA Missense Suppressor from Salmonella enterica Has an Intriguing Mechanism of Action.
[So] Source:Genetics;205(2):577-588, 2017 Feb.
[Is] ISSN:1943-2631
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:While most missense suppressors have very narrow specificities and only suppress the allele against which they were isolated, the sumA missense suppressor from Salmonella enterica serovar Typhimurium is a promiscuous or broad-acting missense suppressor that suppresses numerous missense mutants. The sumA missense suppressor was identified as a glyV tRNA Gly3(GAU/C) missense suppressor that can recognize GAU or GAC aspartic acid codons and insert a glycine amino acid instead of aspartic acid. In addition to rescuing missense mutants caused by glycine to aspartic acid changes as expected, sumA could also rescue a number of other missense mutants as well by changing a neighboring (contacting) aspartic acid to glycine, which compensated for the other amino acid change. Thus the ability of sumA to rescue numerous missense mutants was due in part to the large number of glycine codons in genes that can be mutated to an aspartic acid codon and in part to the general tolerability and/or preference for glycine amino acids in proteins. Because the glyV tRNA Gly3(GAU/C) missense suppressor has also been extensively characterized in Escherichia coli as the mutA mutator, we demonstrated that all gain-of-function mutants isolated in a glyV tRNA Gly3(GAU/C) missense suppressor are transferable to a wild-type background and thus the increased mutation rates, which occur in glyV tRNA Gly3(GAU/C) missense suppressors, are not due to the suppression of these mutants.
[Mh] Termos MeSH primário: Genes Bacterianos
Genes Supressores
Mutação de Sentido Incorreto
RNA de Transferência/genética
Salmonella enterica/genética
[Mh] Termos MeSH secundário: Códon/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Codon); 9014-25-9 (RNA, Transfer)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170530
[Lr] Data última revisão:
170530
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161216
[St] Status:MEDLINE
[do] DOI:10.1534/genetics.116.196550


  10 / 1794 MEDLINE  
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[PMID]:27879964
[Au] Autor:Tian YW; Shen Q; Jiang QF; Wang YX; Li K; Xue HZ
[Ad] Endereço:Department of Hepatobiliary Surgery, Zhengzhou University People's Hospital, Zhengzhou, China.
[Ti] Título:Decreased levels of miR-34a and miR-217 act as predictor biomarkers of aggressive progression and poor prognosis in hepatocellular carcinoma.
[So] Source:Minerva Med;108(2):108-113, 2017 Apr.
[Is] ISSN:1827-1669
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: MicroRNAs (miRNAs) play key roles in tumor development and progression. The aim of this study was to explore the expression levels of miR-34a and miR-217 in hepatocellular carcinoma (HCC) and to further investigate the clinicopathological and prognostic value of miR-34a and miR-217. METHODS: The expression levels of miR-34a and miR-217 were evaluated using quantitative real-time PCR (qRT-PCR). Associations between these miRNAs expression and clinicopathological features were analyzed. Survival rate was determined with Kaplan-Meier and statistically analyzed with the log-rank method between groups. RESULTS: We found that miR-34a expression was significantly downregulated in HCC tissues (P<0.05). Reduced expression of miR-34a was associated with vascular invasion, and advanced TNM stage (P<0.05). Kaplan-Meier revealed that reduced expression of miR-34a was associated with poor overall survival (log-rank test, P<0.05). We found that miR-217 was downregulated in HCC tissues. Decreased expression of miR-217 was remarkably correlated vascular invasion, and advanced TNM stage (P<0.05). Kaplan-Meier analysis and log-rank test showed that HCC patients with low expression of miR-217 was associated with shorter overall survival than patients with high expression (log-rank test, P<0.05). CONCLUSIONS: Our data showed that downregulation of miR-34a and miR-217 was associated with HCC progression and both of them may act as tumor suppressor in HCC.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/metabolismo
Carcinoma Hepatocelular/genética
Neoplasias Hepáticas/genética
MicroRNAs/metabolismo
[Mh] Termos MeSH secundário: Carcinoma Hepatocelular/mortalidade
Carcinoma Hepatocelular/patologia
Progressão da Doença
Regulação para Baixo
Feminino
Genes Supressores
Seres Humanos
Estimativa de Kaplan-Meier
Neoplasias Hepáticas/mortalidade
Neoplasias Hepáticas/patologia
Masculino
Meia-Idade
Invasividade Neoplásica
Prognóstico
Modelos de Riscos Proporcionais
Reação em Cadeia da Polimerase em Tempo Real
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (MIRN217 microRNA, human); 0 (MIRN34 microRNA, human); 0 (MicroRNAs)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170224
[Lr] Data última revisão:
170224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161124
[St] Status:MEDLINE
[do] DOI:10.23736/S0026-4806.16.04616-4



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