Thematische Bibliographien / FTSJ1

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Veröffentlicht am 25. Mai 2024

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Zeitschriftenartikel zum Thema "FTSJ1"

Sun, Yangqing, Qingqing Liu, Shangwei Zhong, Rui Wei und Jun-Li Luo. „Triple-Negative Breast Cancer Intrinsic FTSJ1 Favors Tumor Progression and Attenuates CD8+ T Cell Infiltration“. Cancers 16, Nr. 3 (31.01.2024): 597. http://dx.doi.org/10.3390/cancers16030597.

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FtsJ RNA 2′-O-methyltransferase 1 (FTSJ1) is a member of the methyltransferase superfamily and is involved in the processing and modification of ribosomal RNA. We herein demonstrate that FTSJ1 favors TNBC progression. The knockdown of FTSJ1 inhibits TNBC cell proliferation and development, induces apoptosis of cancer cells, and increases the sensitivity of TNBC cells to T-cell-mediated cytotoxicity. Furthermore, the high expression of FTSJ1 in TNBC attenuates CD8+T cell infiltration in the tumor microenvironment (TME) correlated with poorer prognosis for clinical TNBC patients. In this study, we establish that FTSJ1 acts as a tumor promotor, is involved in cancer immune evasion, and may serve as a potential immunotherapy target in TNBC.

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Brazane, Mira, Dilyana G. Dimitrova, Julien Pigeon, Chiara Paolantoni, Tao Ye, Virginie Marchand, Bruno Da Silva et al. „The ribose methylation enzyme FTSJ1 has a conserved role in neuron morphology and learning performance“. Life Science Alliance 6, Nr. 4 (31.01.2023): e202201877. http://dx.doi.org/10.26508/lsa.202201877.

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FTSJ1 is a conserved human 2′-O-methyltransferase (Nm-MTase) that modifies several tRNAs at position 32 and the wobble position 34 in the anticodon loop. Its loss of function has been linked to X-linked intellectual disability (XLID), and more recently to cancers. However, the molecular mechanisms underlying these pathologies are currently unclear. Here, we report a novelFTSJ1pathogenic variant from an X-linked intellectual disability patient. Using blood cells derived from this patient and other affected individuals carryingFTSJ1mutations, we performed an unbiased and comprehensive RiboMethSeq analysis to map the ribose methylation on all human tRNAs and identify novel targets. In addition, we performed a transcriptome analysis in these cells and found that several genes previously associated with intellectual disability and cancers were deregulated. We also found changes in the miRNA population that suggest potential cross-regulation of some miRNAs with these key mRNA targets. Finally, we show that differentiation of FTSJ1-depleted human neural progenitor cells into neurons displays long and thin spine neurites compared with control cells. These defects are also observed inDrosophilaand are associated with long-term memory deficits. Altogether, our study adds insight into FTSJ1 pathologies in humans and flies by the identification of novel FTSJ1 targets and the defect in neuron morphology.

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von Bohlen und Halbach, Viola, Simone Venz, Simon Nwakor, Christian Hentschker, Elke Hammer, Heike Junker, Andreas Walter Kuss, Oliver von Bohlen und Halbach und Lars Riff Jensen. „Deficiency in FTSJ1 Affects Neuronal Plasticity in the Hippocampal Formation of Mice“. Biology 11, Nr. 7 (05.07.2022): 1011. http://dx.doi.org/10.3390/biology11071011.

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The role of the tRNA methyltransferase FTSJ1 in the brain is largely unknown. We analyzed whether FTSJ1-deficient mice (KO) displayed altered neuronal plasticity. We explored open field behavior (10 KO mice (aged 22–25 weeks)) and 11 age-matched control littermates (WT) and examined mean layer thickness (7 KO; 6 WT) and dendritic spines (5 KO; 5 WT) in the hippocampal area CA1 and the dentate gyrus. Furthermore, long-term potentiation (LTP) within area CA1 was investigated (5 KO; 5 WT), and mass spectrometry (MS) using CA1 tissue (2 each) was performed. Compared to controls, KO mice showed a significant reduction in the mean thickness of apical CA1 layers. Dendritic spine densities were also altered in KO mice. Stable LTP could be induced in the CA1 area of KO mice and remained stable at for at least 1 h, although at a lower level as compared to WTs, while MS data indicated differential abundance of several proteins, which play a role in neuronal plasticity. FTSJ1 has an impact on neuronal plasticity in the murine hippocampal area CA1 at the morphological and physiological levels, which, in conjunction with comparable changes in other cortical areas, might accumulate in disturbed learning and memory functions.

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Carollo, Pietro Salvatore, Marco Tutone, Giulia Culletta, Ignazio Fiduccia, Federica Corrao, Ivana Pibiri, Aldo Di Leonardo et al. „Investigating the Inhibition of FTSJ1, a Tryptophan tRNA-Specific 2′-O-Methyltransferase by NV TRIDs, as a Mechanism of Readthrough in Nonsense Mutated CFTR“. International Journal of Molecular Sciences 24, Nr. 11 (01.06.2023): 9609. http://dx.doi.org/10.3390/ijms24119609.

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Cystic Fibrosis (CF) is an autosomal recessive genetic disease caused by mutations in the CFTR gene, coding for the CFTR chloride channel. About 10% of the CFTR gene mutations are “stop” mutations that generate a premature termination codon (PTC), thus synthesizing a truncated CFTR protein. A way to bypass PTC relies on ribosome readthrough, which is the ribosome’s capacity to skip a PTC, thus generating a full-length protein. “TRIDs” are molecules exerting ribosome readthrough; for some, the mechanism of action is still under debate. We investigate a possible mechanism of action (MOA) by which our recently synthesized TRIDs, namely NV848, NV914, and NV930, could exert their readthrough activity by in silico analysis and in vitro studies. Our results suggest a likely inhibition of FTSJ1, a tryptophan tRNA-specific 2′-O-methyltransferase.

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Angelova, Margarita T., Dilyana G. Dimitrova, Bruno Da Silva, Virginie Marchand, Caroline Jacquier, Cyrinne Achour, Mira Brazane et al. „tRNA 2′-O-methylation by a duo of TRM7/FTSJ1 proteins modulates small RNA silencing in Drosophila“. Nucleic Acids Research 48, Nr. 4 (16.01.2020): 2050–72. http://dx.doi.org/10.1093/nar/gkaa002.

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Abstract 2′-O-Methylation (Nm) represents one of the most common RNA modifications. Nm affects RNA structure and function with crucial roles in various RNA-mediated processes ranging from RNA silencing, translation, self versus non-self recognition to viral defense mechanisms. Here, we identify two Nm methyltransferases (Nm-MTases) in Drosophila melanogaster (CG7009 and CG5220) as functional orthologs of yeast TRM7 and human FTSJ1. Genetic knockout studies together with MALDI-TOF mass spectrometry and RiboMethSeq mapping revealed that CG7009 is responsible for methylating the wobble position in tRNAPhe, tRNATrp and tRNALeu, while CG5220 methylates position C32 in the same tRNAs and also targets additional tRNAs. CG7009 or CG5220 mutant animals were viable and fertile but exhibited various phenotypes such as lifespan reduction, small RNA pathways dysfunction and increased sensitivity to RNA virus infections. Our results provide the first detailed characterization of two TRM7 family members in Drosophila and uncover a molecular link between enzymes catalyzing Nm at specific tRNAs and small RNA-induced gene silencing pathways.

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Dai, Ling, Lianxi Xing, Pingyuan Gong, Kejin Zhang, Xiaocai Gao, Zijian Zheng, Jianping Zhou, Yale Guo, Shaoping Guo und Fuchang Zhang. „Positive association of the FTSJ1 gene polymorphisms with nonsyndromic X-linked mental retardation in young Chinese male subjects“. Journal of Human Genetics 53, Nr. 7 (10.04.2008): 592–97. http://dx.doi.org/10.1007/s10038-008-0287-x.

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Jensen, Lars R., Lillian Garrett, Sabine M. Hölter, Birgit Rathkolb, Ildikó Rácz, Thure Adler, Cornelia Prehn et al. „A mouse model for intellectual disability caused by mutations in the X-linked 2′‑O‑methyltransferase Ftsj1 gene“. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1865, Nr. 9 (September 2019): 2083–93. http://dx.doi.org/10.1016/j.bbadis.2018.12.011.

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Freude, Kristine, Kirsten Hoffmann, Lars-Riff Jensen, Martin B. Delatycki, Vincent des Portes, Bettina Moser, Ben Hamel et al. „Mutations in the FTSJ1 Gene Coding for a Novel S-Adenosylmethionine–Binding Protein Cause Nonsyndromic X-Linked Mental Retardation“. American Journal of Human Genetics 75, Nr. 2 (August 2004): 305–9. http://dx.doi.org/10.1086/422507.

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Fradejas-Villar, Noelia, Simon Bohleber, Wenchao Zhao, Uschi Reuter, Annika Kotter, Mark Helm, Rainer Knoll et al. „The Effect of tRNA[Ser]Sec Isopentenylation on Selenoprotein Expression“. International Journal of Molecular Sciences 22, Nr. 21 (23.10.2021): 11454. http://dx.doi.org/10.3390/ijms222111454.

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Transfer RNA[Ser]Sec carries multiple post-transcriptional modifications. The A37G mutation in tRNA[Ser]Sec abrogates isopentenylation of base 37 and has a profound effect on selenoprotein expression in mice. Patients with a homozygous pathogenic p.R323Q variant in tRNA-isopentenyl-transferase (TRIT1) show a severe neurological disorder, and hence we wondered whether selenoprotein expression was impaired. Patient fibroblasts with the homozygous p.R323Q variant did not show a general decrease in selenoprotein expression. However, recombinant human TRIT1R323Q had significantly diminished activities towards several tRNA substrates in vitro. We thus engineered mice conditionally deficient in Trit1 in hepatocytes and neurons. Mass-spectrometry revealed that hypermodification of U34 to mcm5Um occurs independently of isopentenylation of A37 in tRNA[Ser]Sec. Western blotting and 75Se metabolic labeling showed only moderate effects on selenoprotein levels and 75Se incorporation. A detailed analysis of Trit1-deficient liver using ribosomal profiling demonstrated that UGA/Sec re-coding was moderately affected in Selenop, Txnrd1, and Sephs2, but not in Gpx1. 2′O-methylation of U34 in tRNA[Ser]Sec depends on FTSJ1, but does not affect UGA/Sec re-coding in selenoprotein translation. Taken together, our results show that a lack of isopentenylation of tRNA[Ser]Sec affects UGA/Sec read-through but differs from a A37G mutation.

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Hirata, Akira, Keisuke Okada, Kazuaki Yoshii, Hiroyuki Shiraishi, Shinya Saijo, Kento Yonezawa, Nobutaka Shimizu und Hiroyuki Hori. „Structure of tRNA methyltransferase complex of Trm7 and Trm734 reveals a novel binding interface for tRNA recognition“. Nucleic Acids Research 47, Nr. 20 (05.10.2019): 10942–55. http://dx.doi.org/10.1093/nar/gkz856.

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Abstract The complex between Trm7 and Trm734 (Trm7–Trm734) from Saccharomyces cerevisiae catalyzes 2′-O-methylation at position 34 in tRNA. We report biochemical and structural studies of the Trm7–Trm734 complex. Purified recombinant Trm7–Trm734 preferentially methylates tRNAPhe transcript variants possessing two of three factors (Cm32, m1G37 and pyrimidine34). Therefore, tRNAPhe, tRNATrp and tRNALeu are specifically methylated by Trm7–Trm734. We have solved the crystal structures of the apo and S-adenosyl-L-methionine bound forms of Trm7–Trm734. Small angle X-ray scattering reveals that Trm7–Trm734 exists as a hetero-dimer in solution. Trm7 possesses a Rossmann-fold catalytic domain, while Trm734 consists of three WD40 β-propeller domains (termed BPA, BPB and BPC). BPA and BPC form a unique V-shaped cleft, which docks to Trm7. The C-terminal region of Trm7 is required for binding to Trm734. The D-arm of substrate tRNA is required for methylation by Trm7–Trm734. If the D-arm in tRNAPhe is docked onto the positively charged area of BPB in Trm734, the anticodon-loop is located near the catalytic pocket of Trm7. This model suggests that Trm734 is required for correct positioning of tRNA for methylation. Additionally, a point-mutation in Trm7, which is observed in FTSJ1 (human Trm7 ortholog) of nosyndromic X-linked intellectual disability patients, decreases the methylation activity.

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Dissertationen zum Thema "FTSJ1"

Brazane, Mira. „Functions of the ribose methyltransferase FTSJ1 in regulation of gene expression and neural development“. Electronic Thesis or Diss., Sorbonne université, 2023. http://www.theses.fr/2023SORUS294.

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Dans tous les domaines du vivant, la majorité des ARN de toutes les catégories sont chimiquement modifiés. De nombreuses études au cours des dernières décennies ont permis de montrer que la perte des enzymes de modification des ARN sont à l’origine de nombreuses pathologies, notamment liées au système nerveux. Au cours de ma thèse, j'ai contribué à la compréhension des fonctions de FTSJ1, une enzyme de la famille Trm7 responsable de la 2’-O-méthylation des ARNt sur deux nucléotides de la boucle anticodon dont le Wobble (nucléotide 34). La perte de fonction de FTSJ1 est à l'origine d'une déficience intellectuelle, cependant, les mécanismes moléculaires sous-jacents restent incompris. Mes collègues de laboratoire ont précédemment identifié les orthologues de FTSJ1 chez la drosophile comme régulateurs des voies d’ARN interférence. Au cours de ma thèse, j'ai contribué à la caractérisation d'un nouveau variant pathologique de FTSJ1 et à l'étude des transcriptomes de lymphocytes dérivés de patients atteints de déficience intellectuelle. J'ai également identifié des défauts morphologiques associés à l’inhibition de FTSJ1 dans des neurones immatures humains en culture. De même, le modèle drosophile dépourvu des orthologues de FTSJ1 présente des défauts morphologiques similaires au niveau des jonctions neuromusculaires. Des évaluations cognitives ont montré une réduction drastique de la mémoire à long terme chez tous les mutants. Étant donné la fonction principale des ARNt dans la traduction, j'ai enfin réalisé un ribosome profiling sur les lignées cellulaires dérivées de patients, ainsi qu'une analyse RNAseq. Une analyse de gene ontology a révélé un nombre de gènes dérégulés au niveau traductionnel, principalement impliqués dans l'apprentissage vocal et imitatif. Dans l'ensemble, ces résultats montrent une régulation des gènes de la morphogenèse cérébrale attribués à FTSJ1, ainsi que des défauts morphologiques altérant les cellules neuronales en culture, mais aussi dans le modèle de drosophile muté dans FTSJ1. En perspective, il serait utile d'exploiter ces nouveaux jeux de données de ribosome profiling chez l’homme et la drosophile, en mettant l'accent sur les signatures spécifiques des codons et sur l'efficacité de la traduction par les ARNt substrats de FTSJ1. Ces résultats pourraient conduire à une meilleure compréhension des mécanismes à l’origine de la déficience intellectuelle liée à FTSJ1
RNAs of all the domains of life carry chemical modifications. Extensive studies over the last decades linked the loss of RNA modification enzymes to several pathologies, notably, ones related to the nervous system. During my PhD, I contributed to the understanding of the functions of FTSJ1, a Trm7 family enzyme responsible for tRNA ribose methylation of two nucleotides of the anticodon loop including the Wobble (34th) position. FTSJ1 loss of function causes intellectual disability, however, the mechanisms underlying this condition remain elusive. My colleagues previously identified the orthologs of FTSJ1 in Drosophila as regulators of RNA interference pathways. During my PhD, I contributed to the characterization of a new FTSJ1 pathological variant, and to the study of transcriptomes of patient derived lymphocytes. I also identified morphological defects associated with the loss of FTSJ1 in cultured human immature neurons. Similarly, the Drosophila model lacking the orthologs of FTSJ1 exhibits similar morphological defects in the neuromuscular junctions. Cognitive assessments exhibited drastically reduced long-term memory in all mutant combinations. Given the primary function of tRNAs in translation, I lastly conducted a transcriptome wide profiling of ribosome footprints on patient derived cell lines, together with an RNAseq analysis. A gene ontology analysis revealed a number of deregulated genes at the translational level, primarily involved in vocal and imitative learning. Overall, these results show a substantial regulation of brain morphogenesis genes attributed to FTSJ1, as well as morphological defects altering cultured neural cells, but also in the Drosophila model lacking FTSJ1. As a perspective, exploitation of new ribosome profiling datasets, with an emphasis on codon specific signatures on translation efficiency by tRNA substrates of FTSJ1 could lead to a better understanding of the mechanisms underlying FTSJ1 related intellectual disability

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Olson, Bradley Jesse Stanford Carnahan. „Biochemical analysis of the chloroplast division proteins FtsZ1 and FtsZ2“. Diss., Connect to online resource - MSU authorized users, 2008.

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Thesis (Ph.D.)--Michigan State University. Dept. of Biochemistry and Molecular Biology, 2008.
Title from PDF t.p. (viewed on Mar. 30, 2009) Includes bibliographical references (p. 222-243). Also issued in print.

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Morello, Luis Gustavo 1982. „Caracterização funcional das proteínas NIP7 e FTSJ3 no processamento do RNA ribossomal em células humanas“. [s.n.], 2012. http://repositorio.unicamp.br/jspui/handle/REPOSIP/317176.

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Orientador: Nilson Ivo Tonin Zanchin
Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
Made available in DSpace on 2018-08-20T22:37:29Z (GMT). No. of bitstreams: 1 Morello_LuisGustavo_D.pdf: 80024877 bytes, checksum: 1848ac9901b4322b786b1dcd7a521a69 (MD5) Previous issue date: 2012
Resumo: Estudos prévios realizados em nosso laboratório demonstraram a interação entre as proteínas humanas SBDS e NIP7. SBDS participa da biogênese de ribossomos e sua deficiência está associada à síndrome de Shwachman- Bodian-Diamond. NIP7 é uma proteína conservada e já foi caracterizada em levedura, onde participa da formação da subunidade ribossomal 60S. Neste trabalho, nós investigamos o papel de NIP7 na síntese de ribossomos em células humanas. A depleção de NIP7 revelou defeitos no processamento do pré-rRNA associado à produção do rRNA 18S, causando déficit na formação da subunidade ribossomal 40S. Essa divergência de resultados entre a função de NIP7 em levedura e células humanas é consistente com o fato de que NIP7 humana não complementa levedura deficiente em Nip7p. Ainda, um rastreamento em sistema de duplo-híbrido tendo NIP7 humana como isca revelou parceiros de interação diferentes daqueles reportados para Nip7p em levedura. FTSJ3 foi a parceira isolada com maior frequência. FTSJ3 é a provável ortóloga de Spb1p em levedura, a qual está envolvida na formação da subunidade ribossomal 60S. A associação entre FTSJ3 e NIP7 foi demonstrada por ensaios de pull-down e imunoprecipitação, como sendo dependente de RNA. A co-localização nucleolar e co-sedimentação dessas proteínas em fracionamento em gradiente de sacarose corroboram a associação. Além disso, células humanas deficientes em FTSJ3 revelaram defeitos na via de maturação do rRNA 18S, mesma via afetada pela depleção de NIP7. Em adição, a caracterização proteômica de complexos contendo FTSJ3 e NIP7 revelaram que essas proteínas co-purificam complexos pré-ribossomais. Uma comparação entre o conjunto de proteínas que interagem com Spb1p e as proteínas identificadas nos ensaios de pull-down com FLAG-FTSJ3 revelou que elas apresentam apenas um ortólogo em comum, o qual, incrivelmente, é Nip7/NIP7. Essas observações revelaram diferenças significativas na função desses fatores durante a síntese de ribossomos em levedura e células humanas, adicionando NIP7 e FTSJ3 na lista crescente de fatores com funções divergentes nas vias de processamento do rRNA em levedura e humanos
Abstract: Previous studies from our laboratory have demonstrated the interaction between the SBDS and NIP7 human proteins. SBDS play a role in ribosome biogenesis and its deficiency is associated to the Shwachman-Bodian-Diamond syndrome. NIP7 is a conserved protein and has already been characterized in yeast, where it participates in the 60S ribosomal subunit formation. In this work, we investigated the role of NIP7 in ribosome biogenesis in human cells. NIP7 knockdown caused pre-rRNA processing defects associated to the 18S rRNA maturation, leading to deficiency in 40S ribosomal subunit synthesis. The divergence between NIP7 function in yeast and human cells is further supported by the fact that human NIP7 does not complement yeast deficient in Nip7p. In addition, a two-hybrid screen using human NIP7 as bait revealed interaction partners different from those reported for yeast Nip7p. FTSJ3 was isolated as one of the most frequent human NIP7-interacting candidates. FTSJ3 is a putative ortholog of yeast Spb1p, which has been implicated in 60S ribosomal subunit synthesis. The association between FTSJ3 and NIP7 was showed by pull-down and immunoprecipitation assays as an RNA-dependent interaction. Nucleolar colocalization and co-sedimentation on a sucrose gradiente fractionation corroborate this association. Furthermore, RNAi-mediated knockdown revealed that depletion of FTSJ3 causes pre-rRNA processing defects in the pathway leading to 18S rRNA maturation, the same pathway affected by NIP7 downregulation. In additon, proteomic characterization of FTSJ3- and NIP7- containing complexes showed that these proteins copurify pre-ribosomal complexes. A comparison of the set of Spb1p-interacting proteins with the proteins identified in the pulldown with FLAG-FTSJ3 showed that they share only one ortholog which, incredibly, is Nip7/NIP7. These observations revealed significant differences in the function of these factors during the synthesis of ribosomes in yeast and human cells, adding NIP7 and FTSJ3 to the growing list of factors with different functions in yeast and human rRNA processing pathways
Doutorado
Genetica Animal e Evolução
Doutor em Genetica e Biologia Molecular

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Neumann, Marianne [Verfasser], und P. [Akademischer Betreuer] Nick. „Functional analysis of FtsZ1-2 in the cytoplasm of Physcomitrella patens (Hedw.) B.S.G. / Marianne Neumann. Betreuer: P. Nick“. Karlsruhe : KIT-Bibliothek, 2008. http://d-nb.info/1013721756/34.

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Ringeard, Mathieu. „TRBP recrute une 2’O-méthyltransférase au niveau de l’ARN du Virus de l’Immunodéficience Humaine de type 1 (VIH-1) : mécanisme d’échappement au système immunitaire inné“. Thesis, Montpellier 1, 2013. http://www.theses.fr/2013MON1T020.

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TRBP (TAR RNA Binding Protein), est un facteur activateur de la réplication du Virus de l'Immunodéficience Humaine de type 1 (VIH-1). Cette protéine cellulaire qui interagit avec les ARN double brins est connue pour son rôle crucial dans la voie des miRNA. Isolée pour sa capacité à interagir avec la séquence leader TAR présente à l'extrémité 5' de tous les ARN du VIH-1, TRBP favorise la réplication du VIH-1 au niveau post-transcriptionnel, en partie via l'inhibition de la PKR (Protéine Kinase ARN dépendante).Dans le but de mieux comprendre les mécanismes moléculaires par lesquels TRBP facilite la réplication du VIH-1, le complexe protéique associé à TRBP a été purifié par immunoprécipitation par double affinité et identifié par spectrométrie de masse. En plus des facteurs déjà connus, un nouveau partenaire à activité ARN 2'-O-méthyltransférase (2'-OMTase) potentielle a été copurifié : la protéine FTSJ3. Chez les eucaryotes supérieurs, deux 2'-OMTases permettent la méthylation des ARNm cellulaires au niveau de la position ribose 2'-O- du premier (coiffe 1) et du deuxième nucléotide (coiffe 2). Cette coiffe 1/2 est une signature moléculaire permettant de discriminer les ARNm endogènes et exogènes. Dans la cellule, MDA5, un senseur cytoplasmique, reconnait les ARN exogènes non coiffés et déclenche la production d'interférons (IFNs) de type I pour établir un état antiviral. Pour échapper à la réponse immune innée, certains virus ont développé des mécanismes leur permettant de mimer une coiffe 1/2.Le VIH ne code pas pour une activité 2'-OMTase. Cependant FTSJ3, de par son interaction avec TRBP, se retrouve à proximité de l'extrémité 5' de l'ARN viral. Cette 2'-OMTase méthyle l'ARN TAR in vitro, qui, transfecté dans les cellules monocytaires humaines U937 n'induit plus la production d'IFNs de type I. A l'inverse, le virus VIH-1 produit en l'absence de FTSJ3 déclenche une induction de l'expression des IFNs de type I dépendante de MDA5 dans les cellules U937. L'expression de ce virus est atténuée suite à un défaut d'import nucléaire. Ainsi, ces travaux montrent que la protéine FTSJ3, recrutée au niveau de l'extrémité 5' de l'ARN du VIH-1 par TRBP, facilite la réplication du VIH-1 en assurant la synthèse d'une coiffe 1/2 qui permet au VIH-1 d'échapper à la reconnaissance par le senseur MDA5 et à l'induction des IFNs de type I. Cette étude met en évidence un nouveau mécanisme permettant au VIH-1 d'échapper à la détection par le système d'immunité innée cellulaire
TRBP (TAR RNA Binding Protein) is a cellular RNA binding protein that facilitates the replication of Human Immunodeficiency Virus type 1 (HIV-1). Isolated for its ability to bind HIV-1 TAR sequence present at the 5' end of all HIV-1 RNA, TRBP promotes HIV-1 replication at a post-transcriptional level by counteracting the antiviral activity of the protein kinase R (PKR).To gain more insight on how TRBP enhances HIV-1 replication, TRBP associated factors were purified using tandem immunoaffinity purification and identified by mass spectrometry. In addition to already known associated factors, a new protein with a putative RNA 2'-O-methyltransferase activity (2'OMTases) was copurified: FTSJ3. In higher eukaryotes, cellular mRNA are methylated on 2'-O ribose position on the first (Cap 1) and second nucleotide (Cap 2). This capping provides a molecular signature for the discrimination of endogenous versus exogenous mRNA. In the cell, MDA5, a cytoplasmic sensor, recognizes exogenous uncapped RNA and activate type I interferons (IFNs) production to establish an antiviral state. To evade innate immune response, some viruses have evolved mechanisms to mimics cap 1/2.HIV-1 does not encode a 2'O-MTase activity. However, owing to its interaction with TRBP, FTSJ3 is recruited at the 5' end of the viral genome and methylates TAR RNA in vitro. When capped by FTSJ3, TAR does not induce type I IFNs anymore when transfected in monocytic cell line U937. Conversely, HIV-1 viruses produced in FTSJ3 knock-down cells triggers type I IFNs expression through MDA5 sensing. This virus is attenuated, expressed in low amounts because of a block at the level of HIV-1 nuclear import. This study shows that FTSJ3 is recruited to HIV-1 5' end TAR sequence by TRBP and facilitates HIV-1 replication. HIV-1 RNA capping allows HIV-1 escape from MDA5 sensing and type I IFN induction. This study highlights a new way of HIV-1 escape from innate immune system

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Lai, Cheng-Wei, und 賴政威. „Molecular Cloning and Characterization of Novel Porcine Ftsj1 and Ftsj2 Genes which are Homologous to E. coli Ribosomal RNA Methyltransferase“. Thesis, 2006. http://ndltd.ncl.edu.tw/handle/88169475316129416185.

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碩士
國立中興大學
生命科學系所
94
Abstract An E. coli heat shock protein called RrmJ (ribosomal RNA large subunit methyltransferase J) is responsible for the 2’-O-ribose methylation of A-loop U2552 in the 23S rRNA. Absence of this methlyation causes to reduce either the efficiency of protein synthesis or the growth rate of E. coli. The RrmJ is also a highly conserved protein from eubacteria to mammalia. In human, three closed homologs of RrmJ have been identified and designated as FTSJ1, FTSJ2 and FTSJ3 proteins. In this study, we have cloned two novel porcine Ftsj1 and Ftsj2 full length cDNAs by RT-PCR, degenerated PCR and 3’-RACE, which encoded two polypeptides with 329 and 245 amino acids, respectively. Under bioinformatic analysis, the significantly similarity of porcine FTSJ1 and FTSJ2 to E. coli RrmJ has been demonstrated that both proteins may perform a similar characteristic to RrmJ. Semi-quantitative RT-PCR results showed that porcine Ftsj1 and Ftsj2 mRNA were expressed in all examined thirteen tissues with different levels. Growing piglets were kept at 25oC, 30oC and 35oC thermal-controlled environment for one week and tissue mRNAs were extracted for detection of the Ftsj1 and Ftsj2 genes expression. Using real-time RT-PCR technique, the results of Ftsj1 and Ftsj2 mRNA expression in the thermal-controlled piglet tissues indicate that porcine Ftsj1 and Ftsj2 mRNA expressions were up regulation in only few tissues, and the roles of FTSJ1 and FTSJ2 in mammalia might be different from E. coli under heat shock stress. DNA methylation status was also examined to understand the correlation between Ftsj2 gene methylation and Ftsj2 mRNA downregulation under heat shock stress. The results showed that all the selected tissues are highly methylated in Ftsj2 intron1, and did not regulated the mechanism of Ftsj2 mRNA expression inhibition; conversely, the methylation status was decreased in the tissues where Ftsj2 mRNA were expression increasely. But if Ftsj2 gene still contains other CpG islands, likely promoter region, which involve the regulation of Ftsj2 expression will be study further.

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Johnson, Carol. „In vivo Analysis of the Role of FtsZ1 and FtsZ2 Proteins in Chloroplast Division in Arabidopsis thaliana“. Thesis, 2012. http://hdl.handle.net/1969.1/ETD-TAMU-2012-05-10930.

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Chloroplasts divide by a constrictive fission process that is regulated by FtsZ proteins. Given the importance of photosynthesis and chloroplasts in general, it is important to understand the mechanisms and molecular biology of chloroplast division. An FtsZ gene is known to be of prokaryotic origin and to have been transferred from a symbiont's genome to host genome via lateral transfer. Subsequent duplication of the initial FtsZ gene gave rise to the FtsZ1 and FtsZ2 genes and protein families in eukaryotes. These proteins co-localize mid-chloroplast to form the Z-ring. Z-ring assembly initiates chloroplast division, and it serves as a scaffold for other chloroplast division proteins. Little is known, however, about the FtsZ protein subunit turnover within the Z-ring, the effects of accessory proteins on Z-ring turnover assemblies, as well as the in vivo ultrastructure of the Z-ring in plants. To investigate the Arabidopsis thaliana FtsZ subunit turnover rate within the Z-ring, a section of the Z-ring in the chloroplasts of living plants expressing fluorescently tagged FtsZ1 or FtsZ2 proteins was photobleached and the recovery rate was monitored. The results show that the fluorescence recovery half times for the FtsZ1 and FtsZ2 proteins are 117s and 325s, respectively. This is significant as these data mirror their differences in GTP hydrolysis rates. To elucidate in vivo structure and ultrastructure of the Z-ring, a protocol was established that maintained fluorescence during high pressure freezing, freeze substitution and low temperature embedding. Afterwards, a correlative microscopy approach was employed to visualize and identify fluorescently labeled puncta, circular structures, at the light microscopy level. These puncta were further resolved as mini-rings using optical microscopy eXperimental (OMX) superresolution microscopy. Electron microscopy (EM) analysis imaged mini-rings and filament assemblies comprised of dense subunits. Electron tomography (ET) showed mini-rings composed of protofilaments.

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Konferenzberichte zum Thema "FTSJ1"

MORIMOTO, MURILO GUIMARÃES, RICARDO AMANCIO MALAGONI und ISABELLA PETRUCCI TEIXEIRA RABELO. „ESTUDO DO PROCESSO DE CRISTALIZAÇÃO DO ÁCIDO CÍTRICO“. In XIII Congresso Brasileiro de Engenharia Química em Iniciação Científica. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/cobecic2019-ftsp1.

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Lai, Cheng-Wei, Ken-Yo Lin, Fang-Jiue Liou, Hsiao-Ling Chen, Ju-Chien Cheng und Chuan-Mu Chen. „Abstract 3877: FTSJ2, a putative ribosomal RNA methyltransferase, suppressed cell invasion and migration in cancer cell line“. In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3877.

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Drachev, Vladimir P., Vladimir M. Shalaev, Andrei Buin und Heinz Nakotte. „Quantum-size effect in nonlinear response of metal nanoparticles“. In Frontiers in Optics. Washington, D.C.: OSA, 2004. http://dx.doi.org/10.1364/fio.2004.fthj1.

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Boyd, Robert W., Mathew S. Bigelow, Nick Lepeshkin, Aaron Schweinsberg und Petros Zerom. „Ultraslow and ultrafast light propagation in room-temperature solids“. In Frontiers in Optics. Washington, D.C.: OSA, 2004. http://dx.doi.org/10.1364/fio.2004.ftuj1.

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Kueppers, Franko, Ismail E. Arad, M. Junaid Ansari, Malte Schneiders und Sascha Vorbeck. „System Optimization for 160 Gbit/s Long-Haul Transmission Systems“. In Frontiers in Optics. Washington, D.C.: OSA, 2005. http://dx.doi.org/10.1364/fio.2005.fthj1.

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Fainman, Y., K. Tetz, R. Rokitski, U. Levy, C. H. Tsai, C. H. Chen, L. Pang, M. Nezhad, H. C. Kim und M. Abashin. „Nanophotonic Materials and Devices for Information Systems Integration“. In Frontiers in Optics. Washington, D.C.: OSA, 2005. http://dx.doi.org/10.1364/fio.2005.ftuj1.

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Chipman, Russell A. „Classification of Depolarizing Mueller Matrices“. In Frontiers in Optics. Washington, D.C.: OSA, 2006. http://dx.doi.org/10.1364/fio.2006.fthj1.

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Mandal, Sudeep, Allen Yang und David Erickson. „Micro- and Nanofluid Dynamics in Optofluidic and Nanophotonic Devices (Invited)“. In Frontiers in Optics. Washington, D.C.: OSA, 2006. http://dx.doi.org/10.1364/fio.2006.ftuj1.

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Sazio, Pier J. A., Adrian Amezcua-Correa, Chris E. Finlayson, John R. Hayes, Thomas J. Scheidemantel, Neil F. Baril, Bryan R. Jackson et al. „Electronic and Plasmonic Materials Inside Microstructured Optical Fibers“. In Frontiers in Optics. Washington, D.C.: OSA, 2007. http://dx.doi.org/10.1364/fio.2007.fthj1.

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Mathies, Richard A. „Femtosecond Stimulated Raman Spectroscopy“. In Frontiers in Optics. Washington, D.C.: OSA, 2007. http://dx.doi.org/10.1364/fio.2007.ftuj1.

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