7 results on '"Aubin Thomas"'
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2. De l’ouverture des données publiques à la co-construction des communs numériques : une stratégie partenariale rénovée pour le développement des services publics numériques
- Author
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Saint-Aubin, Thomas, Institut de Recherche juridique de la Sorbonne André Tunc (IRJS), Université Paris 1 Panthéon-Sorbonne (UP1), and Saint-Aubin, Thomas
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[SHS.DROIT]Humanities and Social Sciences/Law ,[SHS.DROIT] Humanities and Social Sciences/Law ,ComputingMilieux_MISCELLANEOUS - Abstract
International audience
- Published
- 2017
3. Coordinate redeployment of PRC1 proteins suppresses tumor formation during Drosophila development
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Anna Delest, Satish Sati, Anne-Marie Martinez, Aubin Thomas, Giacomo Cavalli, Vincent Loubiere, Bernd Schuettengruber, Boyan B. Bonev, Institut de génétique humaine (IGH), Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), and Université de Montpellier (UM)
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0301 basic medicine ,[SDV]Life Sciences [q-bio] ,Polycomb-Group Proteins ,Genes, Insect ,macromolecular substances ,Article ,Histones ,03 medical and health sciences ,Downregulation and upregulation ,Genetics ,Polycomb-group proteins ,Animals ,Drosophila Proteins ,Humans ,Drosophila (subgenus) ,Gene ,ComputingMilieux_MISCELLANEOUS ,Histone Demethylases ,Polycomb Repressive Complex 1 ,[SDV.GEN]Life Sciences [q-bio]/Genetics ,biology ,Cell growth ,Tumor Suppressor Proteins ,fungi ,Histone-Lysine N-Methyltransferase ,biology.organism_classification ,Cell biology ,030104 developmental biology ,Histone ,Larva ,biology.protein ,Drosophila ,PRC1 ,Microtubule-Associated Proteins ,Drosophila Protein - Abstract
Polycomb group proteins form two main complexes, PRC2 and PRC1, which generally coregulate their target genes. Here we show that PRC1 components act as neoplastic tumor suppressors independently of PRC2 function. By mapping the distribution of PRC1 components and trimethylation of histone H3 at Lys27 (H3K27me3) across the genome, we identify a large set of genes that acquire PRC1 in the absence of H3K27me3 in Drosophila larval tissues. These genes massively outnumber canonical targets and are mainly involved in the regulation of cell proliferation, signaling and polarity. Alterations in PRC1 components specifically deregulate this set of genes, whereas canonical targets are derepressed in both PRC1 and PRC2 mutants. In human embryonic stem cells, PRC1 components colocalize with H3K27me3 as in Drosophila embryos, whereas in differentiated cell types they are selectively recruited to a large set of proliferation and signaling-associated genes that lack H3K27me3, suggesting that the redeployment of PRC1 components during development is evolutionarily conserved.
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- 2015
- Full Text
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4. Identification of regulators of the three-dimensional polycomb organization by a microscopy-based genome-wide RNAi screen
- Author
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Thierry Cheutin, Aubin Thomas, Inma González, Giacomo Cavalli, Julio Mateos-Langerak, Institut de génétique humaine (IGH), and Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)
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genetic structures ,SUMO protein ,Polycomb-Group Proteins ,macromolecular substances ,Biology ,Cell Line ,03 medical and health sciences ,0302 clinical medicine ,Gene silencing ,Animals ,Cluster Analysis ,Drosophila Proteins ,Molecular Biology ,Gene ,Psychological repression ,ComputingMilieux_MISCELLANEOUS ,Loss function ,030304 developmental biology ,Genetics ,Cell Nucleus ,[SDV.GEN]Life Sciences [q-bio]/Genetics ,0303 health sciences ,fungi ,Sumoylation ,Cell Biology ,Sumoylation Pathway ,Chromatin ,Cell biology ,Protein Transport ,Drosophila melanogaster ,Gene Ontology ,Phenotype ,Imaginal Discs ,Epigenetic Repression ,Gene Knockdown Techniques ,RNA Interference ,030217 neurology & neurosurgery ,Protein Binding - Abstract
Polycomb group (PcG) proteins dynamically define cellular identities through epigenetic repression of key developmental genes. PcG target gene repression can be stabilized through the interaction in the nucleus at PcG foci. Here, we report the results of a high-resolution microscopy genome-wide RNAi screen that identifies 129 genes that regulate the nuclear organization of Pc foci. Candidate genes include PcG components and chromatin factors, as well as many protein-modifying enzymes, including components of the SUMOylation pathway. In the absence of SUMO, Pc foci coagulate into larger aggregates. Conversely, loss of function of the SUMO peptidase Velo disperses Pc foci. Moreover, SUMO and Velo colocalize with PcG proteins at PREs, and Pc SUMOylation affects its chromatin targeting, suggesting that the dynamic regulation of Pc SUMOylation regulates PcG-mediated silencing by modulating the kinetics of Pc binding to chromatin as well as its ability to form Polycomb foci.
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- 2013
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- View/download PDF
5. Topoisomerase I suppresses genomic instability by preventing interference between replication and transcription
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John De Vos, Laure Crabbe, Anna Jauch, Véronique Pantesco, Yves Pommier, Aubin Thomas, Heidi Holtgreve-Grez, Charles Theillet, Philippe Pasero, Sandie Tuduri, Arnaud Coquelle, Jamal Tazi, Hélène Tourrière, Chiara Conti, Institut de génétique humaine (IGH), Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Institut de recherche en cancérologie de Montpellier (IRCM - U896 Inserm - UM1), CRLCC Val d'Aurelle - Paul Lamarque-Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Montpellier 1 (UM1), Institut de recherche en biothérapie (IRB), Université Montpellier 1 (UM1)-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Université Montpellier 1 - UFR de Médecine (UM1 Médecine), Université Montpellier 1 (UM1), Unité de thérapie cellulaire, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-CHU Saint-Eloi, Institut de Génétique Moléculaire de Montpellier (IGMM), Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM), Institut de génétique humaine ( IGH ), Université de Montpellier ( UM ) -Centre National de la Recherche Scientifique ( CNRS ), Institut de recherche en cancérologie de Montpellier ( IRCM ), Université Montpellier 1 ( UM1 ) -CRLCC Val d'Aurelle - Paul Lamarque-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Université de Montpellier ( UM ), Institut de recherche en biothérapie ( IRB ), Université Montpellier 1 ( UM1 ) -Centre Hospitalier Régional Universitaire [Montpellier] ( CHRU Montpellier ) -Université de Montpellier ( UM ), Montpellier 1 - UFR de Médecine ( UM1 Médecine ), Université Montpellier 1 ( UM1 ), Centre Hospitalier Régional Universitaire [Montpellier] ( CHRU Montpellier ) -CHU Saint-Eloi, and Institut de Génétique Moléculaire de Montpellier ( IGMM )
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DNA re-replication ,DNA Replication ,Chromatin Immunoprecipitation ,Transcription, Genetic ,Eukaryotic DNA replication ,Biology ,Pre-replication complex ,Article ,Genomic Instability ,S Phase ,DNA replication factor CDT1 ,03 medical and health sciences ,0302 clinical medicine ,Replication factor C ,Minichromosome maintenance ,Control of chromosome duplication ,Animals ,ComputingMilieux_MISCELLANEOUS ,030304 developmental biology ,0303 health sciences ,[SDV.GEN]Life Sciences [q-bio]/Genetics ,Cell Biology ,Molecular biology ,Cell biology ,DNA Topoisomerases, Type I ,030220 oncology & carcinogenesis ,biology.protein ,Origin recognition complex ,[ SDV.GEN ] Life Sciences [q-bio]/Genetics - Abstract
Topoisomerase I (Top1) is a key enzyme in functioning at the interface between DNA replication, transcription and mRNA maturation. Here, we show that Top1 suppresses genomic instability in mammalian cells by preventing a conflict between transcription and DNA replication. Using DNA combing and ChIP (chromatin immunoprecipitation)-on-chip, we found that Top1-deficient cells accumulate stalled replication forks and chromosome breaks in S phase, and that breaks occur preferentially at gene-rich regions of the genome. Notably, these phenotypes were suppressed by preventing the formation of RNA-DNA hybrids (R-loops) during transcription. Moreover, these defects could be mimicked by depletion of the splicing factor ASF/SF2 (alternative splicing factor/splicing factor 2), which interacts functionally with Top1. Taken together, these data indicate that Top1 prevents replication fork collapse by suppressing the formation of R-loops in an ASF/SF2-dependent manner. We propose that interference between replication and transcription represents a major source of spontaneous replication stress, which could drive genomic instability during the early stages of tumorigenesis.
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- 2010
6. Analysis of replication profiles reveals key role of RFC-Ctf18 in yeast replication stress response
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Véronique Pantesco, Armelle Lengronne, Philippe Pasero, Aubin Thomas, John De Vos, Laure Crabbe, Institut de génétique humaine (IGH), Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Institut de recherche en biothérapie (IRB), and Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Montpellier 1 (UM1)-Université de Montpellier (UM)
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DNA Replication ,Saccharomyces cerevisiae Proteins ,Mutant ,DNA, Single-Stranded ,Cell Cycle Proteins ,Saccharomyces cerevisiae ,Biology ,03 medical and health sciences ,0302 clinical medicine ,Control of chromosome duplication ,Stress, Physiological ,Structural Biology ,Replication (statistics) ,Hydroxyurea ,Molecular Biology ,ComputingMilieux_MISCELLANEOUS ,030304 developmental biology ,Genetics ,0303 health sciences ,[SDV.GEN]Life Sciences [q-bio]/Genetics ,Replication stress ,Intracellular Signaling Peptides and Proteins ,Budding yeast ,Yeast ,3. Good health ,DNA replication checkpoint ,Phosphorylation ,Carrier Proteins ,030217 neurology & neurosurgery ,DNA Damage - Abstract
Maintenance of genome integrity relies on surveillance mechanisms that detect and signal arrested replication forks. Although evidence from budding yeast indicates that the DNA replication checkpoint (DRC) is primarily activated by single-stranded DNA (ssDNA), studies in higher eukaryotes have implicated primer ends in this process. To identify factors that signal primed ssDNA in Saccharomyces cerevisiae, we have screened a collection of checkpoint mutants for their ability to activate the DRC, using the repression of late origins as readout for checkpoint activity. This quantitative analysis reveals that neither RFC(Rad24) and the 9-1-1 clamp nor the alternative clamp loader RFC(Elg1) is required to signal paused forks. In contrast, we found that RFC(Ctf18) is essential for the Mrc1-dependent activation of Rad53 and for the maintenance of paused forks. These data identify RFC(Ctf18) as a key DRC mediator, potentially bridging Mrc1 and primed ssDNA to signal paused forks.
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- 2010
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- View/download PDF
7. Erratum: Topoisomerase I suppresses genomic instability by preventing interference between replication and transcription
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Sandie Tuduri, Laure Crabbé, Chiara Conti, Hélène Tourrière, Heidi Holtgreve-Grez, Anna Jauch, Véronique Pantesco, John De Vos, Aubin Thomas, Charles Theillet, Yves Pommier, Jamal Tazi, Arnaud Coquelle, Philippe Pasero, Institut de génétique humaine (IGH), Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Institut de recherche en cancérologie de Montpellier (IRCM - U896 Inserm - UM1), CRLCC Val d'Aurelle - Paul Lamarque-Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Montpellier 1 (UM1), Institut de recherche en biothérapie (IRB), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Montpellier 1 (UM1)-Université de Montpellier (UM), Université Montpellier 1 - UFR de Médecine (UM1 Médecine), Université Montpellier 1 (UM1), Unité de thérapie cellulaire, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-CHU Saint-Eloi, Institut de Génétique Moléculaire de Montpellier (IGMM), and Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM)
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[SDV.GEN]Life Sciences [q-bio]/Genetics ,0303 health sciences ,03 medical and health sciences ,0302 clinical medicine ,030220 oncology & carcinogenesis ,Cell Biology ,ComputingMilieux_MISCELLANEOUS ,030304 developmental biology - Abstract
International audience
- Published
- 2010
- Full Text
- View/download PDF
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