Literatura académica sobre el tema "Méthylation intragénique de l'ADN"
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Artículos de revistas sobre el tema "Méthylation intragénique de l'ADN"
Jeanpierre, M. "L'ADN peut-il se passer de la méthylation ?" médecine/sciences 10, n.º 3 (1994): 351. http://dx.doi.org/10.4267/10608/2619.
Texto completoDragic, D., S. L. Chang, K. Ennour-Idrissi, F. Durocher, G. Severi y C. Diorio. "127 - Consommation d'alcool et méthylation de l'ADN dans le sang : une revue systématique". Revue d'Épidémiologie et de Santé Publique 70 (agosto de 2022): S162. http://dx.doi.org/10.1016/j.respe.2022.06.095.
Texto completoGouri, Adel, Mohamed Bouchareb, Aoulia Dekaken, Ahmed Aimen Bentorki, Mohamed Chefrour, Régis Guieu y Sadek Benharkat. "Epigenetics and pathogenesis of type 2 diabetes". Batna Journal of Medical Sciences (BJMS) 2, n.º 1 (30 de junio de 2015): 56–59. http://dx.doi.org/10.48087/bjmstf.2015.2113.
Texto completoChatti, Abdelwaheb y Ahmed Landoulsi. "L'état de la méthylation de l'ADN régule la virulence et la réponse au stress chez Salmonella". Comptes Rendus Biologies 331, n.º 9 (septiembre de 2008): 648–54. http://dx.doi.org/10.1016/j.crvi.2008.06.002.
Texto completoCOUSTHAM, Vincent, Charlotte ANDRIEUX, Chloé CERUTTI, Anne COLLIN, Ingrid DAVID, Julie DEMARS, Guillaume DEVAILLY et al. "Epigénétique, gènes et environnement : quelle importance pour les pratiques d’élevage et les méthodes de sélection des volailles ?" INRAE Productions Animales 36, n.º 4 (20 de diciembre de 2023): 7384. http://dx.doi.org/10.20870/productions-animales.2023.36.4.7384.
Texto completoMERSCH, Marjorie, Sarah-Anne DAVID, Anaïs VITORINO CARVALHO, Sylvain FOISSAC, Anne COLLIN, Frédérique PITEL y Vincent COUSTHAM. "Apports du séquençage haut-débit sur la connaissance de l'épigénome aviaire". INRA Productions Animales 31, n.º 4 (23 de enero de 2019): 325–36. http://dx.doi.org/10.20870/productions-animales.2018.31.4.2372.
Texto completoTesis sobre el tema "Méthylation intragénique de l'ADN"
Yi, Jia. "The Role of Convergent Transcription in Regulating Alternative Splicing : Targeted Epigenetic Modification via Repurposed CRISPR/Cas9 System and Its Impact on Alternative Splicing Modulation". Electronic Thesis or Diss., Sorbonne université, 2020. http://www.theses.fr/2020SORUS382.
Texto completoAlternative splicing of precursor RNA is a co-transcriptional process that affects the vast majority of human genes and contributes to protein diversity. Dysregulation of such process is implicated in various diseases, including tumorigenesis. However, the mechanisms regulating these processes were still to be characterized. In this study, we showed that perturbations of alternative splicing correlated with dysregulations of convergent transcription and DNA methylation. Convergent transcription could be generated between pairs of neighboring genes in opposite orientation, or between intragenic enhancers and their host gene. CENPO and ADCY3 was identified as a convergent transcription gene pair. We found, in a tumor progression model of breast cancer, that the splicing change of the ADCY3 variant exon22 correlated with an increase of its transcription that went against that of CENPO. By using targeted transcription repression system CRISPRi, we demonstrated that downregulating the transcription of CENPO could not reverse the alternative splicing alteration of ADCY3 in cancer cells (DCIS). An active intragenic enhancer was identified in the intron16 of CD44, at the downstream of its alternative exons. By using targeted transcription activation system CRISPRa, we showed that upregulating the transcription of CD44 could not alter the alternative splicing of CD44 in DCIS cells. These results suggest that convergent transcription modulation through changes of promoter activity does not alter the alternative splicing of ADCY3 and CD44 in DCIS cells. However, through replacing the intragenic enhancer by an inducible promoter, we found that intragenic transcription activation increased the inclusion level of several alternative exons of CD44 in HCT116 cells. This result suggested that local convergent transcription could have a direct impact on the alternative splicing of CD44. Furthermore, by using targeted DNA methylation system CRISPR/dCas9-DNMT3b, we showed that DNA methylation at variant exons could directly modify CD44 alternative splicing. This thesis work also explored the limitation and feasibility of studying alternative splicing with repurposed CRISPR systems
Bender-Osmani, Ambre. "Méthylation de l'ADN et identité cellulaire : fonctions de la méthylation de l'ADN dans les lignages gamétiques et hématopoïétiques chez la souris". Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ102.
Texto completoThe methylation of DNA is a well-known epigenetic mark. It consists in adding a methyl group to a cytosine producing the 5-methylcytosine (5mC). This is catalysed by the DNA methyltransferase (DNMT) family: DNMT1, DNMT3A and DNMT3B. Little is known about the changes in DNA methylation that follow lineage decisions in the embryo and how these contribute, establish or maintain cellular identities. We are addressing these questions using as a model the specification of mouse primordial germ cells (PGCs) and mouse hematopoietic stem cells (HSCs) in the mouse embryo. We generate the first genome-wide maps of 5mC during their development. These maps highlight two waves of DNA methylation in PGCs. The first one takes place between E9,5 and E13,5, where the genome demethylates while the second one corresponds to a remethylation phase only in male PGCs between E14,5 and E17,5. Nevertheless, some regions, notably the transposable elements, are resistant to this demethylation wave. We demonstrate the implication of DNMT1 and UHRF2 in maintaining the 5mC on these regions using transgenic mice presenting specific deletion in PGCs. In HSCs, the 5mC maps highlight two wave of DNA methylation. The first one correlates with the first appearance of the HSCs in early embryos while the second one corresponds to their migration to the bone marrow and seems to act as a definitive lock for their hematopoietic identity. Using transgenic mice presenting specific deletions in HSCs, we prove the implication of DNMT3A and DNMT3B in hematopoietic stem cells, with a major role in locking HSC identity of DNMT3B during the first wave and a DNMT3A during the second one respectively
Filion, Guillaume. "Caractérisation fonctionnelle d'un répresseur transcriptionnel spécifique de l'ADN méthylé". Paris 11, 2007. http://www.theses.fr/2007PA112337.
Texto completoDelpu, Yannick. "Méthylation de l'ADN et expression des microARNs dans la carcinogénèse pancréatique". Toulouse 3, 2013. http://thesesups.ups-tlse.fr/2128/.
Texto completoPancreatic cancer is the fourth leading cause of cancer death in Western countries. This cancer involves changes in DNA methylation patterns and overexpression of enzymes responsible for its implementation : the DNA methyltransferases. However, the exact role of these proteins in carcinogenesis remains to be proven. We first aimed to determine the changing in the DNA methylation pattern through the study of the expression of a specific microRNA : miR- 148a. We confirmed the repression of miR- 148a by DNA hypermethylation in several cell lines derived from pancreatic cancer as well as in human tumor samples, and we shown the usefulness of this mark in the differential diagnosis between pancreatic cancer and chronic pancreatitis. We also evaluated the therapeutic potential of miR- 148a gene transfer in vitro and in vivo. We observed no significant changes in the behavior of cells / tumors overexpressing miR- 148a. This indicates that its repression is a minor alteration accompanying carcinogenesis rather than a crucial phenomenon of tumor development. Finally, we extended our study to determine whether the single overexpression of DNA methyltransferases can transform normal pancreatic cells. We observed that the stable overexpression of these proteins significantly affects the behavior of cells in vitro, their methylation patterns and gene expression. These results strongly suggest that DNA methylation facilitates carcinogenesis, but is not sufficient to trigger the formation of tumors. This work contributes to a better understanding of pancreatic carcinogenesis, the role of DNA methylation and open new horizons for the potential oncogenic role of DNA methylation
Caillet, Nina. "Rôle de la méthylation de l'ADN et des microARN dans les lymphomes T anaplasiques à grandes cellules ALK positifs". Thesis, Toulouse 3, 2019. http://www.theses.fr/2019TOU30139.
Texto completoAnaplastic Large Cell Lymphoma (ALCL) is the most common pediatric T lymphoma. Mostly CD4(+), in about 80% of cases ALCL expresses the oncogenic tyrosine kinase NPM-ALK. Using a high-throughput sequencing of human NPM-ALK(+) ALCL treated with decitabine, or transfected with siRNA against ALK, I have shown that NPM-ALK, STAT3, and methyltransferase DNA 1 (DNMT1), induce hypermethylation of the MIR125 genes. In vitro, inhibition of topoisomerase II activity by doxorubicin inhibits the fixation of DNMT1 at the MIR125B gene promoter. Using microRNA-biotinyled purification we identified BAK1 mRNA as target of miR125b. In primary ALCL, miR125b and the pro-apoptotic protein BAK1 were correlated with relapse risk after chemotherapy. Moreover, I developed cellular NPM-ALK(+) ALCLmodels by transduced human CD4 lymphocytes (CD4/NPM-ALK(+)). Integrative analysis of methylome and transcriptome showed that CD4/NPM-ALK(+) and primary NPM-ALK(+) ALCLhave similar profile, close to thymic precursors but different to normal CD4 lymphocytes. Preliminary miRNome analysis also suggests that CD4/NPM-ALK (+) are different from normal CD4 cells. In addition, we observed a expression decrease by DNA methylation of transcription factors essential to the differentiation of T precursors. An increase of expression of pluripotency transcription factors is also observed. Coherent way, we noted a correlation between the hypomethylation of the EPAS1 gene promoter and the overexpression of the HIF2a protein which affects the differentiation and survival of hematopoietic precursors. We have highlighted the therapeutic potential of HIF2a antagonists as potential treatments. Altogether, our findings suggest that NPM-ALK through DNA methylation i) represses expression of microRNA implicated in chemotherapy resistanceand ii) could restore progenitor-like features in mature peripheral T-cells in keeping with a thymic progenitor-like pattern
Greiner, Vanille. "Epigénétique et méthylation de l'ADN : étude des mécanismes d'interaction du domaine SRA de UHRF1 avec l'ADN hémi-méthylé". Thesis, Strasbourg, 2012. http://www.theses.fr/2012STRAJ107/document.
Texto completoThe UHRF1 protein plays a key role in the maintenance and transmission of epigenetic modifications. Duringthe replication process, it recruits the DNA methyltransferase Dnmt1 to hemi-methylated CpG sites via itsSRA (SET and RING Associated) domain, promoting the duplication of the methylation profiles. Thetridimensional structure of the SRA/DNA complex revealed that the protein induces a base-flipping of themethylcytosine that enables a specific anchoring of the protein to hemi-methylated sites facilitating therecruitment of Dnmt1 to this strategic position. In this context, our project was aimed to further understand themechanism of interaction of the SRA domain with hemi-methylated DNA. To this end, oligonucleotideduplexes were labeled by 2-aminopurine, a fluorescent nucleoside analogue sensitive to environment, atvarious positions close to the single hemi-methylated CpG recognition site. Steady-state and time-resolvedfluorescence spectroscopy measurements of these duplexes bound to the SRA domain enabled us to sitespecificallycharacterize the conformational changes induced by the binding of this domain. In agreement withthe tridimensional structure of the SRA/DNA complex, our data suggest that the SRA domain is able to flip themethylcytosine while preserving the structure of the surrounding bases in the duplex. The SRA domain wasshown to bind with the same mechanism to hemi-methylated, fully-methylated and non-methylated duplexes.Our data suggest the UHRF1 protein plays a role of “reader” that scans the DNA sequence for hemimethylatedsites
Bosviel, Rémy. "Méthylation de l'ADN, phyto-oestrogènes et cancer du sein et de l'ovaire". Thesis, Clermont-Ferrand 1, 2011. http://www.theses.fr/2011CLF1MM21/document.
Texto completoBreast cancer is the most common cancer and the leading cause of cancer death among women worldwide [1]. Many factors contribute to the development of this disease and the BRCA1 and BRCA2 genes are particularly involved. Indeed, mutations in these two oncosuppressors are responsible for 5 to 10% of hereditary breast cancers [2]. In addition, a decrease in their expression is found in a large number of sporadic breast cancers [3]. Hereditary mutations of the BRCA1 and BRCA2 genes are also at the origin of ovarian cancers [4]. This cancer is much less common than breast cancer, but it is associated with a poor prognosis. In addition to these genetic factors, hormonal factors also seem to be involved in the processes of breast and ovarian carcinogenesis, but also environmental factors and more particularly food. Soybean consumption, which is common in some parts of Asia, is thought to reduce the risk of developing breast cancer in Asian countries compared to Western countries. It is the phytoestrogens contained in soy that act, thanks to their similarity of structure with the 17-β-estradiol of the woman [5]. Soy phytoestrogens may also affect the development of ovarian cancer since it is an estrogen-dependent cancer, such as breast cancer. The Nutrition and Cancer team of the Department of Oncogenetics at the Jean Perrin Center is studying the potentially preventative effects of soy phytoestrogens in the carcinogenesis process. A first study, conducted within the team, showed that the expression of BRCA1 and BRCA2 genes in the mammary gland could be modulated by the consumption of soy in ovariectomized rats [6]. Also, transcriptomic studies have shown that the consequences of the inactivation of BRCA1 and BRCA2 oncosuppressors by the use of a small interfering RNA in mammary cells could be countered by treatment with soy phytoestrogens [7, 8]. Following the emergence of studies showing the effects of soy phytoestrogens on DNA methylation, and the presence of methylation in the BRCA1 and BRCA2 gene promoter in sporadic breast cancers, we wanted to see if the soy phytoestrogens could directly affect the methylation of these two oncosuppressors, which we have previously identified in breast and ovarian cancers
Menon, Yoann. "Etude des effets pharmacologiques d'inhibiteurs non nucléosidiques de la méthylation de l'ADN". Thesis, Toulouse 3, 2016. http://www.theses.fr/2016TOU30004/document.
Texto completoEpigenetic modifications participate to the control of gene expression. Methylation of deoxycytidines (dC) in the DNA was shown to play a key role in epigenetic regulation in mammals. It is the most stable epigenetic mark and occurs at CpG sites, which are grouped in islands and essentially located in promoters, repeated sequences and CpG island shores. Hypermethylation of promoters induces gene silencing while hypomethylation is associated to gene expression. Enzymes responsible for DNA methylation are the DNA methyltransferases (DNMTs). Two families of catalyticallyactive DNMTs have been identified: DNMT1, mainly responsible for DNA methylation maintenance during replication; and DNMT3A and 3B that perform de novo DNA methylation and support maintenance. Alteration of DNA methylation patterns lead to various diseases such as cancer. Cancerous cells often present aberrant DNA methylation, in particular a specific hypermethylation of tumor suppressor genes is observed. Restoring their expression by inhibition of DNA methylation represents an attractive therapeutic strategy. Several DNMTs inhibitors have been described. Two nucleoside analogs are FDA approved to treat leukemia: 5-azacytidine (VidazaTM) and 5-azadeoxycytidine (Dacogene(r)). Our laboratory develops since several years new inhibitors of DNMT, non-nucleoside analogs, targeting the catalytic site. Here, I studied the pharmacological effects of these DNMTs catalytic inhibitors using several cancer cell lines (leukemia, lymphoma and colon cancer) and different technologies to follow DNA methylation, chromatin accessibility, histone modifications and gene expression. Since epigenetic therapies aim at the reprogramming of cancer cells, I explored the long-term modifications induced by the compounds. We show that these novel compounds are potent inhibitors of DNMT3A and able to induce the expression of a reporter gene (luciferase) under the control of a methylated CMV promoter by demethylation of the promoter and opening of the chromatin. Finally, these new DNMTs inhibitors demethylate the promoter region of tumor suppressor genes and induce their re-expression
Auclair, Ghislain. "Identification de cibles et régulateurs de la méthylation de l'ADN chez la souris". Thesis, Strasbourg, 2015. http://www.theses.fr/2015STRAJ061.
Texto completoDNA methylation is an epigenetic modification which is established during embryonic development on the mammalian genome. In my thesis, I determined the kinetics of DNA methylation acquisition on the mouse genome during early embryogenesis, and determined the specific and redundant roles of the DNA methyltransferases DNMT3a and DNMT3b in this process. I also studied the roles of two factors involved in setting up DNA methylation in embryos. First, I determined that the G9a enzyme plays an essential role for the in vivo repression and DNA methylation of specific genomic sites, including in particular the CpG island promoters of germline genes. Second, the study of the E2F6 factor allowed me to show that this protein is also involved in recruiting DNA methylation at a set of germline gene promoters than are distinct from those regulated by G9a
Payelleville, Amaury. "Etude de la méthylation de l'ADN chez la bactérie pathogène d'insectes Photorhabdus luminescens". Thesis, Montpellier, 2018. http://www.theses.fr/2018MONTG063/document.
Texto completoPhotorhabdus luminescens is an Enterobacteriaceae found in soils in symbiosis with a nematode from the genus Heterorhabditis. This nemato-bacterial complex is highly pathogenic against insect pest crops and so used in biocontrol. The nematode enters into the insect and releases Photorhabdus in the hemolymph of the insect. Photorhabdus multiplies and produces diverse virulence factors as toxins. Insect die from septicemia and both nematodes and bacteria feed on the nutrients in the cadaver. Once nutrients are lacking, the nematodes and the bacteria reassociate and exit from the cadaver to find new insects to infect. Photorhabdus is switching between pathogenic and symbiotic state. This bacterium displays phenotypic heterogeneity as we observe subpopulations coexisting in a same bacterial culture. Phenotypic heterogeneity can be explained by epigenetic mechanisms such as DNA methylation. In Enterobacteriaceae, Dam methyltransferase is broadly distributed. It methylates the adenine of GATC sites. Dam is involved in post-replicative mismatch repair, cell-cycle regulation and also gene transcription regulation. This methyltransferase can be in competition with some transcriptional regulators. Depending on which will bind first on the promoter region, gene will be expressed or not, leading to the rise of two subpopulations. This thesis aims to understand roles of Dam in Photorhabdus luminescens. Overexpression of the methyltransferase leads to a decrease in motility and pathogenicity of Photorhabdus Dam+ strain whereas it increases biofilms formation. A transcriptomic analysis (RNAseq) revealed differential expression of genes involved in the observed phenotypes. Symbiosis establishment does not seem to be strongly impacted in Dam+ strain as the only difference observed when compared to the nematode associated with the control strain is the same as with bacteria alone (a delayed virulence). A methylome analysis was also done (screening of all methylated sites in the genome using SMRT sequencing) in several growth conditions which revealed that DNA methylation is stable over growth kinetics. Dam+ strain methylome analysis confirmed the hypothesis that Dam overexpression increases GATC methylation over the genome. Comparative analysis of methylome and RNAseq experiments between control and Dam+ strains highlighted several common genes. In fact, some genes are differentially expressed between both strains and also have GATC sites differentially methylated in their promoter region. Their transcription regulation by methylation is a future aim and may give some explanation for a part of the phenotypes observed in Photorhabdus luminescens