Search

Your search keyword '"Montibus, Bertille"' showing total 26 results
Start Over Author "Montibus, Bertille"
26 results on '"Montibus, Bertille"'

3. Imprinting control regions (ICRs) are marked by mono-allelic bivalent chromatin when transcriptionally inactive

Author

Maupetit-Méhouas, Stéphanie, Montibus, Bertille, Nury, David, Tayama, Chiharu, Wassef, Michel, Kota, Satya, Fogli, Anne, Campos, Fabiana Cerqueira, Hata, Kenichiro, Feil, Robert, Margueron, Raphaël, Nakabayashi, Kazuhiko, Court, Franck, and Arnaud, Philippe

Subjects
Quantitative Biology - Genomics, Quantitative Biology - Molecular Networks
Abstract

Parental allele-specific expression of imprinted genes is mediated by imprinting control regions (ICRs) that are constitutively marked by DNA methylation imprints on the maternal or paternal allele. Mono-allelic DNA methylation is strictly required for the process of imprinting and has to be faithfully maintained during the entire lifespan. While the regulation of DNA methylation itself is well understood, the mechanisms whereby the opposite allele remains unmethylated are unclear. Here, we show that in the mouse, at maternally methylated ICRs, the paternal allele, which is constitutively associated with H3K4me2/3, is marked by default by H3K27me3 when these ICRs are transcriptionally inactive, leading to the formation of a bivalent chromatin signature. Our data suggest that at ICRs, chromatin bivalency has a protective role by ensuring that DNA on the paternal allele remains unmethylated and protected against spurious and unscheduled gene expression. Moreover , they provide the proof of concept that, beside pluripotent cells, chromatin bivalency is the default state of transcriptionally inactive CpG island promoters , regardless of the developmental stage, thereby contributing to protect cell identity.

Published
2018
Full Text
View/download PDF

4. Biallelic non-productive enhancer-promoter interactions precede imprinted expression of Kcnk9 during mouse neural commitment

Author

Rojas, Cecilia Rengifo, primary, Cercy, Jil, additional, Perillous, Sophie, additional, Gonthier-Guéret, Céline, additional, Montibus, Bertille, additional, Maupetit-Méhouas, Stéphanie, additional, Espinadel, Astrid, additional, Dupré, Marylou, additional, Hong, Charles C., additional, Hata, Kenichiro, additional, Nakabayashi, Kazuhiko, additional, Plagge, Antonius, additional, Bouschet, Tristan, additional, Arnaud, Philippe, additional, Vaillant, Isabelle, additional, and Court, Franck, additional

Published
2024
Full Text
View/download PDF

7. Biallelic non-productive enhancer-promoter interaction precedes imprinted expression of Kcnk9 during mouse neural commitment

Author

Rojas, Cecilia Rengifo, primary, Cercy, Jil, additional, Perillous, sophie, additional, Gonthier-Gueret, Celine, additional, Montibus, Bertille, additional, Maupetit-Mehouas, Stephanie, additional, Espinadel, Astrid, additional, Dupre, Marylou, additional, Hong, Charles C, additional, Hata, Kenichiro, additional, Nakabayashi, Kazuhiko, additional, Plagge, Antonius, additional, Bouschet, Trsitan, additional, arnaud, philippe, additional, Vaillant, Isabelle, additional, and Court, Franck, additional

Published
2023
Full Text
View/download PDF

11. Enhancer-promoter interactions are reconfigured through the formation of long-range multiway chromatin hubs as mouse ES cells exit pluripotency

Author

Lando, David, primary, Ma, Xiaoyan, additional, Cao, Yang, additional, Jartseva, Aleksandra, additional, Stevens, Timothy J, additional, Boucher, Wayne, additional, Reynolds, Nicola, additional, Montibus, Bertille, additional, Hall, Dominic, additional, Lackner, Andreas, additional, Ragheb, Ramy, additional, Leeb, Martin, additional, Hendrich, Brian, additional, and Laue, Ernest D, additional

Published
2023
Full Text
View/download PDF

13. The Long Non-Coding RNA HOXA-AS2 Promotes Proliferation of Glioma Stem Cells and Modulates Their Inflammation Pathway Mainly through Post-Transcriptional Regulation

Author

Le Boiteux, Elisa, primary, Guichet, Pierre-Olivier, additional, Masliantsev, Konstantin, additional, Montibus, Bertille, additional, Vaurs-Barriere, Catherine, additional, Gonthier-Gueret, Céline, additional, Chautard, Emmanuel, additional, Verrelle, Pierre, additional, Karayan-Tapon, Lucie, additional, Fogli, Anne, additional, Court, Franck, additional, and Arnaud, Philippe, additional

Published
2022
Full Text
View/download PDF

16. Imprinted Gene Expression and Function of the Dopa Decarboxylase Gene in the Developing Heart

Author

Prickett, Adam R., primary, Montibus, Bertille, additional, Barkas, Nikolaos, additional, Amante, Samuele M., additional, Franco, Maurício M., additional, Cowley, Michael, additional, Puszyk, William, additional, Shannon, Matthew F., additional, Irving, Melita D., additional, Madon-Simon, Marta, additional, Ward, Andrew, additional, Schulz, Reiner, additional, Baldwin, H. Scott, additional, and Oakey, Rebecca J., additional

Published
2021
Full Text
View/download PDF

20. TET3 controls the expression of the H3K27me3 demethylase Kdm6b during neural commitment

Author

Montibus, Bertille, primary, Cercy, Jil, additional, Bouschet, Tristan, additional, Charras, Amandine, additional, Maupetit-Méhouas, Stéphanie, additional, Nury, David, additional, Gonthier-Guéret, Céline, additional, Chauveau, Sabine, additional, Allegre, Nicolas, additional, Chariau, Caroline, additional, Hong, Charles C., additional, Vaillant, Isabelle, additional, Marques, C. Joana, additional, Court, Franck, additional, and Arnaud, Philippe, additional

Published
2020
Full Text
View/download PDF

21. Imprinting control regions (ICRs) are marked by mono-allelic bivalent chromatin when transcriptionally inactive

Author

Maupetit-M��houas, St��phanie, Montibus, Bertille, Nury, David, Tayama, Chiharu, Wassef, Michel, Kota, Satya, Fogli, Anne, Campos, Fabiana Cerqueira, Hata, Kenichiro, Feil, Robert, Margueron, Rapha��l, Nakabayashi, Kazuhiko, Court, Franck, Arnaud, Philippe, Université Clermont Auvergne [2017-2020] (UCA [2017-2020]), Institut des cellules souches pour le traitement et l'étude des maladies monogéniques (I-STEM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Généthon-Université d'Évry-Val-d'Essonne (UEVE), Hôpital Lariboisière, Department of Pathology, University of Paris 7 - Denis Diderot, Faculty of Medicine, Assistance Publique - Hôpitaux de Paris, Institut de Génétique Moléculaire de Montpellier (IGMM), Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM), Interactions génétiques et cellulaires au cours de la différenciation, Université d'Auvergne - Clermont-Ferrand I (UdA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of Maternal-Fetal Biology, National Research Institute for Child Health and Development, Interfakultäres Institut für Biochemie, Eberhard Karls Universität Tübingen = Eberhard Karls University of Tuebingen, Endocrinologie moléculaire et cellulaire des cancers, Université Montpellier 1 (UM1)-Institut National de la Santé et de la Recherche Médicale (INSERM), Génétique, Reproduction et Développement (GReD), Centre National de la Recherche Scientifique (CNRS)-Université Clermont Auvergne [2017-2020] (UCA [2017-2020])-Institut National de la Santé et de la Recherche Médicale (INSERM), Université d'Évry-Val-d'Essonne (UEVE)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Généthon, Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Clermont Auvergne [2017-2020] (UCA [2017-2020])-Centre National de la Recherche Scientifique (CNRS), Graduate School of Information Science, Nara Institute of Science and Technology, Risques, Ecosystèmes, Vulnérabilité, Environnement, Résilience (RECOVER), and Institut national de recherche en sciences et technologies pour l'environnement et l'agriculture (IRSTEA)

Subjects
Genomics (q-bio.GN), Molecular Networks (q-bio.MN), FOS: Biological sciences, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Quantitative Biology - Genomics, Quantitative Biology - Molecular Networks, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, [SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, [SDV.BBM.MN]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular Networks [q-bio.MN], [SDV.CAN]Life Sciences [q-bio]/Cancer
Abstract

International audience; Parental allele-specific expression of imprinted genes is mediated by imprinting control regions (ICRs) that are constitutively marked by DNA methy-lation imprints on the maternal or paternal allele. Mono-allelic DNA methylation is strictly required for the process of imprinting and has to be faithfully maintained during the entire lifespan. While the regulation of DNA methylation itself is well understood, the mechanisms whereby the opposite allele remains unmethylated are unclear. Here, we show that in the mouse, at maternally methylated ICRs, the paternal allele, which is constitutively associated with H3K4me2/3, is marked by default by H3K27me3 when these ICRs are transcriptionally inactive, leading to the formation of a bivalent chromatin signature. Our data suggest that at ICRs, chromatin bivalency has a protective role by ensuring that DNA on the paternal allele remains unmethylated and protected against spurious and unscheduled gene expression. Moreover , they provide the proof of concept that, beside pluripotent cells, chromatin bivalency is the default state of transcriptionally inactive CpG island promoters , regardless of the developmental stage, thereby contributing to protect cell identity.

Published
2016

23. Imprinting control regions (ICRs) are marked by mono-allelic bivalent chromatin when transcriptionally inactive

Author

Maupetit-Méhouas, Stéphanie, primary, Montibus, Bertille, additional, Nury, David, additional, Tayama, Chiharu, additional, Wassef, Michel, additional, Kota, Satya K., additional, Fogli, Anne, additional, Cerqueira Campos, Fabiana, additional, Hata, Kenichiro, additional, Feil, Robert, additional, Margueron, Raphael, additional, Nakabayashi, Kazuhiko, additional, Court, Franck, additional, and Arnaud, Philippe, additional

Published
2015
Full Text
View/download PDF

24. Cancer-associated mutations in the protrusion-targeting region of p190RhoGAP impact tumor cell migration.

Author

Binarné, Fabien, Bidaud-Meynard, Aurélien, Magnan, Laure, Piquet, Léo, Montibus, Bertille, Chabadel, Anne, Saltel, Frédéric, Lagrée, Valérie, and Moreau, Violaine

Subjects
*CELL migration, *CANCER cell migration, *GTPASE-activating protein, *CARRIER proteins, *LIVER cancer
Abstract

Spatiotemporal regulation of RhoGTPases such as RhoA is required at the cell leading edge to achieve cell migration. p190RhoGAP (p190A) is the main negative regulator of RhoA and localizes to membrane protrusions, where its GTPase-activating protein (GAP) activity is required for directional migration. In this study, we investigated the molecular processes responsible for p190A targeting to actin protrusions. By analyzing the subcellular localization of truncated versions of p190A in hepatocellular carcinoma cells, we identified a novel functional p190A domain: the protrusion localization sequence (PLS) necessary and sufficient for p190A targeting to leading edges. Interestingly, the PLS is also required for the negative regulation of p190A RhoGAP activity. Further, we show that the F-actin binding protein cortactin binds the PLS and is required for p190A targeting to protrusions. Lastly, we demonstrate that cancer-associated mutations in PLS affect p190A localization and function, as well as tumor cell migration. Altogether, our data unveil a new mechanism of regulation of p190A in migrating tumor cells. [ABSTRACT FROM AUTHOR]

Published
2016
Full Text
View/download PDF

25. The Nucleosome Remodelling and Deacetylation complex coordinates the transcriptional response to lineage commitment in pluripotent cells.

Author

Montibus B, Ragheb R, Diamanti E, Dunn SJ, Reynolds N, and Hendrich B

Subjects
Nucleosomes, Cell Differentiation genetics, Mi-2 Nucleosome Remodeling and Deacetylase Complex genetics, Transcription Factors genetics, Transcription Factors metabolism, DNA-Binding Proteins metabolism
Abstract

As cells exit the pluripotent state and begin to commit to a specific lineage they must activate genes appropriate for that lineage while silencing genes associated with pluripotency and preventing activation of lineage-inappropriate genes. The Nucleosome Remodelling and Deacetylation (NuRD) complex is essential for pluripotent cells to successfully undergo lineage commitment. NuRD controls nucleosome density at regulatory sequences to facilitate transcriptional responses, and also has been shown to prevent unscheduled transcription (transcriptional noise) in undifferentiated pluripotent cells. How these activities combine to ensure cells engage a gene expression program suitable for successful lineage commitment has not been determined. Here, we show that NuRD is not required to silence all genes. Rather, it restricts expression of genes primed for activation upon exit from the pluripotent state, but maintains them in a transcriptionally permissive state in self-renewing conditions, which facilitates their subsequent activation upon exit from naïve pluripotency. We further show that NuRD coordinates gene expression changes, which acts to maintain a barrier between different stable states. Thus NuRD-mediated chromatin remodelling serves multiple functions, including reducing transcriptional noise, priming genes for activation and coordinating the transcriptional response to facilitate lineage commitment., Competing Interests: Competing interests Sara-Jane Dunn was an employee at Microsoft Research during this study and is currently employed at DeepMind. Neither Microsoft Research nor DeepMind have directed any aspect of the study nor exerted any commercial rights over the results. The authors declare no conflicts of interest., (© 2024. Published by The Company of Biologists Ltd.)

Published
2024
Full Text
View/download PDF

26. Imprinting control regions (ICRs) are marked by mono-allelic bivalent chromatin when transcriptionally inactive.

Author

Maupetit-Méhouas S, Montibus B, Nury D, Tayama C, Wassef M, Kota SK, Fogli A, Cerqueira Campos F, Hata K, Feil R, Margueron R, Nakabayashi K, Court F, and Arnaud P

Subjects
Animals, Cells, Cultured, Chromatin genetics, DNA (Cytosine-5-)-Methyltransferases genetics, DNA (Cytosine-5-)-Methyltransferases metabolism, DNA Methylation, Embryonic Stem Cells physiology, Female, Gene Expression Regulation, Male, Mice, Inbred C57BL, Mice, Mutant Strains, Organ Specificity, Promoter Regions, Genetic, Alleles, Chromatin metabolism, Genomic Imprinting
Abstract

Parental allele-specific expression of imprinted genes is mediated by imprinting control regions (ICRs) that are constitutively marked by DNA methylation imprints on the maternal or paternal allele. Mono-allelic DNA methylation is strictly required for the process of imprinting and has to be faithfully maintained during the entire life-span. While the regulation of DNA methylation itself is well understood, the mechanisms whereby the opposite allele remains unmethylated are unclear. Here, we show that in the mouse, at maternally methylated ICRs, the paternal allele, which is constitutively associated with H3K4me2/3, is marked by default by H3K27me3 when these ICRs are transcriptionally inactive, leading to the formation of a bivalent chromatin signature. Our data suggest that at ICRs, chromatin bivalency has a protective role by ensuring that DNA on the paternal allele remains unmethylated and protected against spurious and unscheduled gene expression. Moreover, they provide the proof of concept that, beside pluripotent cells, chromatin bivalency is the default state of transcriptionally inactive CpG island promoters, regardless of the developmental stage, thereby contributing to protect cell identity., (© The Author(s) 2015. Published by Oxford University Press on behalf of Nucleic Acids Research.)

Published
2016
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results