Thematische Bibliographien / Epigenetic reprograming

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Auswahl der wissenschaftlichen Literatur zum Thema „Epigenetic reprograming“

Autor: Grafiati

Veröffentlicht am 25. Mai 2024

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Zeitschriftenartikel zum Thema "Epigenetic reprograming"

Lameirinhas, Ana, Vera Miranda-Gonçalves, Rui Henrique und Carmen Jerónimo. „The Complex Interplay between Metabolic Reprogramming and Epigenetic Alterations in Renal Cell Carcinoma“. Genes 10, Nr. 4 (02.04.2019): 264. http://dx.doi.org/10.3390/genes10040264.

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Renal cell carcinoma (RCC) is the most common malignancy affecting the kidney. Current therapies are mostly curative for localized disease, but do not completely preclude recurrence and metastization. Thus, it is imperative to develop new therapeutic strategies based on RCC biological properties. Presently, metabolic reprograming and epigenetic alterations are recognized cancer hallmarks and their interactions are still in its infancy concerning RCC. In this review, we explore RCC biology, highlighting genetic and epigenetic alterations that contribute to metabolic deregulation of tumor cells, including high glycolytic phenotype (Warburg effect). Moreover, we critically discuss available data concerning epigenetic enzymes’ regulation by aberrant metabolite accumulation and their consequences in RCC emergence and progression. Finally, we emphasize the clinical relevance of uncovering novel therapeutic targets based on epigenetic reprograming by metabolic features to improve treatment and survival of RCC patients.

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Aguirre-Vázquez, Alain, Luis A. Salazar-Olivo, Xóchitl Flores-Ponce, Ana L. Arriaga-Guerrero, Dariela Garza-Rodríguez, María E. Camacho-Moll, Iván Velasco, Fabiola Castorena-Torres, Nidheesh Dadheech und Mario Bermúdez de León. „5-Aza-2′-Deoxycytidine and Valproic Acid in Combination with CHIR99021 and A83-01 Induce Pluripotency Genes Expression in Human Adult Somatic Cells“. Molecules 26, Nr. 7 (29.03.2021): 1909. http://dx.doi.org/10.3390/molecules26071909.

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A generation of induced pluripotent stem cells (iPSC) by ectopic expression of OCT4, SOX2, KLF4, and c-MYC has established promising opportunities for stem cell research, drug discovery, and disease modeling. While this forced genetic expression represents an advantage, there will always be an issue with genomic instability and transient pluripotency genes reactivation that might preclude their clinical application. During the reprogramming process, a somatic cell must undergo several epigenetic modifications to induce groups of genes capable of reactivating the endogenous pluripotency core. Here, looking to increase the reprograming efficiency in somatic cells, we evaluated the effect of epigenetic molecules 5-aza-2′-deoxycytidine (5AZ) and valproic acid (VPA) and two small molecules reported as reprogramming enhancers, CHIR99021 and A83-01, on the expression of pluripotency genes and the methylation profile of the OCT4 promoter in a human dermal fibroblasts cell strain. The addition of this cocktail to culture medium increased the expression of OCT4, SOX2, and KLF4 expression by 2.1-fold, 8.5-fold, and 2-fold, respectively, with respect to controls; concomitantly, a reduction in methylated CpG sites in OCT4 promoter region was observed. The epigenetic cocktail also induced the expression of the metastasis-associated gene S100A4. However, the epigenetic cocktail did not induce the morphological changes characteristic of the reprogramming process. In summary, 5AZ, VPA, CHIR99021, and A83-01 induced the expression of OCT4 and SOX2, two critical genes for iPSC. Future studies will allow us to precise the mechanisms by which these compounds exert their reprogramming effects.

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Habel, Nadia, Najla El-Hachem, Frédéric Soysouvanh, Hanene Hadhiri-Bzioueche, Serena Giuliano, Sophie Nguyen, Pavel Horák et al. „FBXO32 links ubiquitination to epigenetic reprograming of melanoma cells“. Cell Death & Differentiation 28, Nr. 6 (18.01.2021): 1837–48. http://dx.doi.org/10.1038/s41418-020-00710-x.

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AbstractUbiquitination by serving as a major degradation signal of proteins, but also by controlling protein functioning and localization, plays critical roles in most key cellular processes. Here, we show that MITF, the master transcription factor in melanocytes, controls ubiquitination in melanoma cells. We identified FBXO32, a component of the SCF E3 ligase complex as a new MITF target gene. FBXO32 favors melanoma cell migration, proliferation, and tumor development in vivo. Transcriptomic analysis shows that FBXO32 knockdown induces a global change in melanoma gene expression profile. These include the inhibition of CDK6 in agreement with an inhibition of cell proliferation and invasion upon FBXO32 silencing. Furthermore, proteomic analysis identifies SMARC4, a component of the chromatin remodeling complexes BAF/PBAF, as a FBXO32 partner. FBXO32 and SMARCA4 co-localize at loci regulated by FBXO32, such as CDK6 suggesting that FBXO32 controls transcription through the regulation of chromatin remodeling complex activity. FBXO32 and SMARCA4 are the components of a molecular cascade, linking MITF to epigenetics, in melanoma cells.

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Bui, L. C., A. V. Evsikov, D. R. Khan, C. Archilla, N. Peynot, A. Hénaut, D. Le Bourhis, X. Vignon, J. P. Renard und V. Duranthon. „Retrotransposon expression as a defining event of genome reprograming in fertilized and cloned bovine embryos“. REPRODUCTION 138, Nr. 2 (August 2009): 289–99. http://dx.doi.org/10.1530/rep-09-0042.

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Genome reprograming is the ability of a nucleus to modify its epigenetic characteristics and gene expression pattern when placed in a new environment. Low efficiency of mammalian cloning is attributed to the incomplete and aberrant nature of genome reprograming after somatic cell nuclear transfer (SCNT) in oocytes. To date, the aspects of genome reprograming critical for full-term development after SCNT remain poorly understood. To identify the key elements of this process, changes in gene expression during maternal-to-embryonic transition in normal bovine embryos and changes in gene expression between donor cells and SCNT embryos were compared using a new cDNA array dedicated to embryonic genome transcriptional activation in the bovine. Three groups of transcripts were mostly affected during somatic reprograming: endogenous terminal repeat (LTR) retrotransposons and mitochondrial transcripts were up-regulated, while genes encoding ribosomal proteins were downregulated. These unexpected data demonstrate specific categories of transcripts most sensitive to somatic reprograming and likely affecting viability of SCNT embryos. Importantly, massive transcriptional activation of LTR retrotransposons resulted in similar levels of their transcripts in SCNT and fertilized embryos. Taken together, these results open a new avenue in the quest to understand nuclear reprograming driven by oocyte cytoplasm.

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Pilsner, J. Richard, Mikhail Parker, Oleg Sergeyev und Alexander Suvorov. „Spermatogenesis disruption by dioxins: Epigenetic reprograming and windows of susceptibility“. Reproductive Toxicology 69 (April 2017): 221–29. http://dx.doi.org/10.1016/j.reprotox.2017.03.002.

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Merino, Aimee, Bin Zhang, Philip Dougherty, Xianghua Luo, Jinhua Wang, Bruce R. Blazar, Jeffrey S. Miller und Frank Cichocki. „Chronic stimulation drives human NK cell dysfunction and epigenetic reprograming“. Journal of Clinical Investigation 129, Nr. 9 (12.08.2019): 3770–85. http://dx.doi.org/10.1172/jci125916.

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Zhang, Zhiren, Yanhui Zhai, Xiaoling Ma, Sheng Zhang, Xinglan An, Hao Yu und Ziyi Li. „Down-Regulation of H3K4me3 by MM-102 Facilitates Epigenetic Reprogramming of Porcine Somatic Cell Nuclear Transfer Embryos“. Cellular Physiology and Biochemistry 45, Nr. 4 (2018): 1529–40. http://dx.doi.org/10.1159/000487579.

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Background/Aims: Aberrantly high levels of H3K4me3, caused by incomplete epigenetic reprogramming, likely cause a low efficiency of somatic cell nuclear transfer (SCNT). Smal molecule inhibitors aimed at epigenetic modification can be used to improve porcine SCNT embryo development. In this study, we examined the effects of MM-102, an H3K4 histone methyltransferase inhibitor, on porcine SCNT preimplantation embryos to investigate the mechanism by which H3K4 methylation regulated global epigenetic reprograming during SCNT. Methods: MM-102 was added to the SCNT embryos culture system and the global levels of various epigenetic modifications were measured by immunofluorescence (IF) staining and were quantified by Image J software. Relative genes expression levels were detected by quantitative real-time PCR. Results: MM-102 (75 μM) treatment reduced global H3K4, H3K9 methylation and 5mC levels especially at the zygotic gene activation (ZGA) and blastocyst stages. MM-102 treatment mainly down-regulated a series of DNA and histone methyltransferases, and up-regulated a number of hitone acetyltransferases and transcriptional activators. Furthermore, MM-102 treatment positively regulated the mRNA expression of genes related to pluripotency (OCT4, NANOG, CDX2) and apoptosis (BCL2). Conclusion: Down-regulation of H3K4me3 with MM-102 rescued aberrant gene expression patterns of a series of epigenetic chromatin modification enzymes, pluripotent and apoptotic genes at the ZGA and blastocyst stages, thereby greatly improving porcine SCNT efficiency and blastocyst quality, making them more similar to in vivo embryos (IVV).

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Amsalem, Zohar, Tasleem Arif, Anna Shteinfer-Kuzmine, Vered Chalifa-Caspi und Varda Shoshan-Barmatz. „The Mitochondrial Protein VDAC1 at the Crossroads of Cancer Cell Metabolism: The Epigenetic Link“. Cancers 12, Nr. 4 (22.04.2020): 1031. http://dx.doi.org/10.3390/cancers12041031.

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Carcinogenesis is a complicated process that involves the deregulation of epigenetics, resulting in cellular transformational events, such as proliferation, differentiation, and metastasis. Most chromatin-modifying enzymes utilize metabolites as co-factors or substrates and thus are directly dependent on such metabolites as acetyl-coenzyme A, S-adenosylmethionine, and NAD+. Here, we show that using specific siRNA to deplete a tumor of VDAC1 not only led to reprograming of the cancer cell metabolism but also altered several epigenetic-related enzymes and factors. VDAC1, in the outer mitochondrial membrane, controls metabolic cross-talk between the mitochondria and the rest of the cell, thus regulating the metabolic and energetic functions of mitochondria, and has been implicated in apoptotic-relevant events. We previously demonstrated that silencing VDAC1 expression in glioblastoma (GBM) U-87MG cell-derived tumors, resulted in reprogramed metabolism leading to inhibited tumor growth, angiogenesis, epithelial–mesenchymal transition and invasiveness, and elimination of cancer stem cells, while promoting the differentiation of residual tumor cells into neuronal-like cells. These VDAC1 depletion-mediated effects involved alterations in transcription factors regulating signaling pathways associated with cancer hallmarks. As the epigenome is sensitive to cellular metabolism, this study was designed to assess whether depleting VDAC1 affects the metabolism–epigenetics axis. Using DNA microarrays, q-PCR, and specific antibodies, we analyzed the effects of si-VDAC1 treatment of U-87MG-derived tumors on histone modifications and epigenetic-related enzyme expression levels, as well as the methylation and acetylation state, to uncover any alterations in epigenetic properties. Our results demonstrate that metabolic rewiring of GBM via VDAC1 depletion affects epigenetic modifications, and strongly support the presence of an interplay between metabolism and epigenetics.

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Mani, Sneha, und Monica Mainigi. „Embryo Culture Conditions and the Epigenome“. Seminars in Reproductive Medicine 36, Nr. 03/04 (Mai 2018): 211–20. http://dx.doi.org/10.1055/s-0038-1675777.

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AbstractAssisted reproductive technologies (ARTs) lead to an increased risk for pregnancy complications, congenital abnormalities, and specific imprinting disorders. Epigenetic dysfunction is thought to be one common mechanism which may be affecting these outcomes. The timing of multiple ART interventions overlaps with developmental time periods that are particularly vulnerable to epigenetic change. In vitro embryo culture is known to impact blastocyst development, in vitro fertilization (IVF) success rates, as well as neonatal outcomes. Embryo culture, in contrast to other procedures involved in ART, is obligatory, and has the highest potential for causing alterations in epigenetic reprograming. In this review, we summarize progress that has been made in exploring the effects of embryo culture, culture media, and oxygen tension on epigenetic regulation in the developing embryo. In humans, it is difficult to isolate the role of embryo culture on epigenetic perturbations. Therefore, additional well-controlled animal studies isolating individual exposures are necessary to minimize the epigenetic effects of modifiable factors utilized during ART. Findings from these studies will likely not only improve IVF success rates but also reduce the risk of adverse perinatal outcomes.

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Byrne, Kristen A., Hamid Beiki, Christopher K. Tuggle und Crystal L. Loving. „β-glucan induced training and tolerance: alterations to primary monocytes“. Journal of Immunology 200, Nr. 1_Supplement (01.05.2018): 59.17. http://dx.doi.org/10.4049/jimmunol.200.supp.59.17.

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Abstract In mice and humans, exposure to β-glucan can induce epigenetic reprograming in monocytes resulting in enhanced responses to heterologous agonists. Epigenetic reprograming is the basis for innate memory, which includes both decreased immune responsiveness (innate tolerance) and increased responsiveness (innate training). As a valuable food animal and medically relevant species, we sought to understand the phenotypic and mechanistic alterations induced by β-glucan on swine cells to develop methods to enhance health while limiting antibiotic usage. Thus, primary porcine monocytes were stimulated with β-glucan from S. cerevisiae or C. albicans, rested for 5 d, and then restimulated with lipopolysaccharide (LPS; TLR 4 agonist) or Pam3CSK4 (synthetic triacylated lipopeptide; TLR 2 agonist) to determine trained or tolerant phenotype (increase or decrease in cytokine production relative to unstimulated controls). Zymosan (β-glucan from S. cerevisiae) primed monocytes exhibited a tolerant phenotype (decreased IL-1β and TNF-α production compared to controls) when restimulated with LPS or Pam3CSK4. However, β-glucan from C. albicans (the primary β-glucan used in mouse and human studies) primed porcine monocytes for increased cytokine production after LPS and Pam3CSK4 stimulation, an indication of trained immunity. Epigenetic analysis of the accessibility of the genome to transposase (ATAC-sequencing) showed changes in promoter peaks with treatment, providing insight into mechanisms of tolerance versus training. These data indicate that β-glucan can induce both training and tolerance in porcine monocytes, but the source and purity of β-glucan likely impacts innate memory.

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Dissertationen zum Thema "Epigenetic reprograming"

Bagci, Hakan. „Epigenetic reprogramming and DNA demethylation“. Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/45352.

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Embryonic development begins with fertilization of the egg, a progressive process that gives rise to the zygote and subsequently to the formation of somatic tissues. Normally once cells acquire a fate, it is stably maintained. Conversion back to a multipotent state occurs rarely in-vivo, but can be achieved experimentally by inducing ‘reprogramming’. In this study I am looking at the epigenetic mechanisms that underlie reprogramming and, in particular, DNA methylation and demethylation. To address this I am taking advantage of the cellular fusion system. Fusion of pluripotent cells with differentiated cells results in the formation of transient heterokaryon and hybrid cells, where the somatic partner is efficiently reprogrammed. This gives me the opportunity to monitor early and late events in pluripotent conversion, in which global remodelling of chromatin and changes in DNA methylation occur. Here, I examine changes in DNA methylation that are induced at imprinted loci and pluripotency-associated genes when somatic cells are fused with either mouse embryonic stem (ES) or embryonic germ (EG) cells. I focus on defining the factors and order of events that accompany reprogramming. I show that acquisition of pluripotency is an early process occurring at the heterokaryon stage, and is followed by imprint erasure later in hybrids. However reprogramming of imprinting is only induced by EG, but not ES cells, and it requires sequential steps of 5-methylcytosine oxidation mediated by Tet proteins and nucleotide exchange upon several rounds of DNA synthesis. I provide evidence that Tet proteins are dispensable for pluripotent reprogramming using CRISPR-Cas9 genome editing to abrogate the expression of both Tet1 and Tet2. This result suggests that either DNA demethylation can occur without TET activity (implying a redundancy with other demethylating agents and routes), or that DNA demethylation is not required for inducing pluripotency. Finally, I describe how CRISPR/Cas9 approaches were used to demonstrate that non-canonical Wnt signalling components are downstream targets of JARID2 in ES cells.

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Hajkova, Petra. „Epigenetic reprogramming in mouse germ cells“. [S.l. : s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=970526938.

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Rao, Venkata Lakshmi Prakruthi. „Epigenetic Reprogramming at the Th2 Locus“. University of Cincinnati / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1543838686940608.

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Ribeiro, Lemos Pereira Carlos Filipe. „Epigenetic events underlying somatic cell reprogramming“. Thesis, Imperial College London, 2008. http://hdl.handle.net/10044/1/4439.

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Although differentiated cells normally retain cell-type-specific gene expressionpatterns throughout their lifetime, cell identity can sometimes be modified or reversedin vivo by transdifferentiation, or experimentally through cell fusion or by nucleartransfer. Several studies have illustrated the importance of chromatin remodelling, DNAdemethylation and dominant transcriptional factor expression for changes in lineageidentity. Here the epigenetic mechanisms required to ?reset? genome function wereinvestigated using experimental heterokaryons.To examine the epigenetic changes that are required for the dominantconversion of lymphocytes to muscle, I generated stable heterokaryons betweenhuman B-lymphocytes and mouse C2C12 myotubes. I show that lymphocyte nucleiadopt an architecture resembling that of muscle and initiate the expression of musclespecificgenes in the same temporal order as developing muscle. The establishment ofthis novel gene expression program is coordinated with the shutdown of severallymphocyte-associated genes. Interestingly, inhibition of histone deacetylase (HDAC)activity during reprogramming selectively blocks the silencing of lymphocyte-specificgenes but does not prevent the establishment of muscle-specific gene expression.In order to reprogram somatic cells to pluripotency, I fused human Blymphocytesand mouse embryonic stem (ES) cells. The conversion of human cells isinitiated rapidly, occurring in heterokaryons before nuclear fusion. Reprogramming ofhuman lymphocytes by mouse ES cells elicits the expression of a human ES-specificgene expression profile in which endogenous hSSEA4, hFgf receptors and ligands areexpressed while factors that are characteristic of mouse ES cells, such as Bmp4 andLif receptor are not. Using genetically engineered mouse ES cells I demonstrate thatsuccessful reprogramming requires the expression of Oct4, but importantly, does notrequire Sox2, a factor implicated as critical for the induction of pluripotency. Followingreprogramming, mOct4 becomes dispensable for maintaining the multi-potent state ofhybrid cells. Finally, I have examined the reprogramming potential of embryonic germ(EG), embryonic carcinoma (EC) and ES cells deficient for the Polycomb repressivecomplex 2 (PRC2) proteins Eed, Suz12 and Ezh2. While EC and EG cells share theability to reprogram human lymphocytes with ES cells, the lack of Polycomb proteinsabolishes reprogramming. Thus, the repressive chromatin mark (H3K27 methylation)catalysed by PRC2 play a crucial role in keeping ES cells with full reprogrammingcapacity. Collectively my results underscore the importance of chromatin events duringcell fate reprogramming.

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Hajkova, Petra. „Epigenetic reprogramming in mouse germ cells“. Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2004. http://dx.doi.org/10.18452/15020.

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Bei Säugerkeimzellen, Zygoten und Embryos in frühen Stadien kommt der epigenetischen Neuprogammierung eine außergewöhnlich wichtige Rolle in der Regulation der Genomfunktionen in entscheidenden Entwicklungsstadien zu. Die epigenetische Neuprogrammierung in Keimzellen löscht zuerst die Imprinting-Markierungen und Epi-Mutationen und stellt dann geschlechtsspezifische Markierungen (genomische Prägung) wieder her. Die vorliegende Arbeit bezieht sich auf das Löschen epigenetischer Modifikationen in primordialen Mauskeimzellen (primordial germ cells (PGCs)) zwischen dem 10.5 bis 13.5 Tag nach der Befruchtung. Entgegen früheren Annahmen zeigen unsere Ergebnisse, daß primordiale Mauskeimzellen (PGCs) beim Eintritt in die embryonalen Keimdrüsen noch immer DNS Methylierungsmarker besitzen, die ähnlich dem Marker in somatischen Zellen sind. Kurz nach dem Eintritt in die Keimdrüsen werden die DNS Methylierungsmarker, die in Verbindung mit geprägten und nicht geprägten Genen stehen, gelöscht. Für die Mehrzahl der Gene beginnt die Löschung der Marker in männlichen und weiblichen Embryos gleichzeitig und ist innerhalb eines Entwicklungstages abgeschlossen. Diese Kinetik deutet auf einen aktiven Demethylierungsprozess hin, initiiert durch ein somatisches Signal, ausgehend von der embryonalen Keimdrüse. Der Zeitpunkt der Neuprogrammierung in den primordialen Keimzellen ist entscheidend, da er sicherstellt, daß Keimzellen beiden Geschlechts einen epigenetisch äquivalenten Status erhalten, bevor sie geschlechtsspezifisch ausdifferenzieren und anschließend neu elterlich geprägt werden. Vollständiges Verständnis des Prozesses der Neuprogrammierung der Keimzellen ist nicht nur im Hinblick auf genomisches Imprinting wichtig, sondern auch für die Erforschung von Mechanismen für die Wiederherstellung von omnipotenten Zellen bei Klonierung und Stammzellenerhaltung.
Epigenetic reprogramming in mammalian germ cells, zygote and early embryos, plays a crucial role in regulating genome functions at critical stages of development. Germ line epigenetic reprogramming assures erasure of all the imprinting marks and epi-mutations and establishment of new sex-specific gametic imprints. The presented work focuses on the erasure of epigenetic modifications that occur in mouse primordial germ cells (PGCs) between day 10.5 to 13.5 post coitum (dpc). Contrary to previous assumptions, our results show that as they enter the genital ridge the PGCs still possess DNA methylation marks comparable to those found in somatic cells. Shortly after the entry of PGCs into the gonadal anlagen the DNA methylation marks associated with imprinted and non-imprinted genes are erased. For most genes the erasure commences simultaneously in PGCs of both male and female embryos and is completed within only one day of development. The kinetics of this process indicates that is an active demethylation process initiated by a somatic signal emanating from the stroma of the genital ridge. The timing of reprogramming in PGCs is crucial since it ensures that germ cells of both sexes acquire an equivalent epigenetic state prior to the differentiation of the definitive male and female germ cells in which, new parental imprints are established subsequently. Complete understanding of the germline reprogramming processes is important not only in the light of genomic imprinting but also for resolving other mechanisms connected with restoring cellular totipotency, such as cloning and stem cell derivation.

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Dura, Mathilde. „Critical and different roles of DNA methylation in male germ cell development“. Electronic Thesis or Diss., Sorbonne université, 2021. http://www.theses.fr/2021SORUS187.

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La méthylation de l'ADN, associée à la répression des gènes et des éléments transposables (ET), joue un rôle essentiel dans la spermatogenèse. Le méthylome des futurs gamètes est reprogrammé : les profils de méthylation somatiques sont effacés, des profils spécifiques des cellules germinales sont établis. Trois de novo ADN méthyltransférases (DNMT) sont essentielles à la méthylation de l'ADN des cellules germinales mâles chez la souris : les enzymes DNMT3C et DNMT3A et leur cofacteur DNMT3L. Il a été montré que DNMT3C est l'enzyme qui méthyle sélectivement les ET les plus jeunes évolutivement. Cependant, les cibles et la fonction de DNMT3A étaient encore inconnues. Je me suis donc intéressée aux rôles de DNMT3A et DNMT3C dans la régulation épigénétique de la spermatogénèse. J'ai démontré (projet 1) une division de travail remarquable : alors que DNMT3C empêche les ET d'interférer avec la méiose, DNMT3A méthyle largement le génome, à l'exception des ET dépendants de DNMT3C. J'ai découvert que les cellules souches spermatogoniales (CSS) mutantes pour Dnmt3A ont perdu leur potentiel de différentiation à cause de l’activation erronée d’enhancers qui imposent un programme génétique de cellules souches. Ce travail révèle une nouvelle fonction de la méthylation de l'ADN dans la fertilité mâle. En parallèle (projet 2), j’ai étudié la nature de la spécificité de reconnaissance des jeunes ET par DNMT3C. Ces séquences présentent une dynamique chromatinienne unique: d’abord un profil bivalent de type H3K4me3-H3K9me3 qui évolue vers un enrichissement H3K9me3 exclusif. Mon travail a ainsi fourni des éléments nouveaux pour comprendre le rôle de la méthylation de l’ADN en reproduction
DNA methylation, associated with gene or transposable element (TE) repression, plays a key role in spermatogenesis. During germ cell development, their methylome is reprogrammed: somatic patterns are erased and germ cell-specific patterns are established. Three de novo DNA methyltransferases (DNMTs) are essential for shaping male germ cell DNA methylation in mice: DNMT3C and DNMT3A enzymes and DNMT3L co-factor. DNMT3C was shown to selectively methylate young TEs. However, the targets and function of DNMT3A was still unknown. During my PhD, I investigated the interplay between DNMT3A and DNMT3C in the epigenetic regulation of spermatogenesis. First (project 1), I reported a striking division of labor: while DNMT3C prevents TEs from interfering with meiosis, DNMT3A broadly methylates the genome—except DNMT3C-dependent TEs—and controls spermatogonial stem cell (SSC) plasticity. By single-cell RNA-seq and chromatin states profiling, I found that Dnmt3A mutant SSCs cannot differentiate due to spurious enhancer activation that enforces a stem cell gene program. I thus demonstrated a novel function for DNA methylation for SSC differentiation and life-long spermatogenesis supply. Second (project 2), I investigated the chromatin determinants of DNMT3C specificity towards young TEs. I found that these sequences present unique dynamics: first a bivalent H3K4me3-H3K9me3 enrichment, followed by a switch to H3K9me3-only. H3K9me3-enrichment was also a hallmark of the sequences that gain DNA methylation upon ectopic DNMT3C expression in cultured embryonic stem cells. As a whole, my work provided novel insights into the complexity of DNA methylation-based control of reproduction

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Oksuz, Samet. „Targeting IL-4 locus for epigenetic reprogramming“. University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1423581203.

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Yong, Qian Yu. „A screen for modifiers of epigenetic reprogramming“. Thesis, Queensland University of Technology, 2011. https://eprints.qut.edu.au/50955/1/Qian_Yu_Yong_Thesis.pdf.

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Epigenetic modifiers are the proteins involved in establishing and maintaining the epigenome of an organism. They are particularly important for development. Changes in epigenetic modifiers have been shown be lethal, or cause diseases. Our laboratory has developed an ENU mutagenesis screen to produce mouse mutants displaying altered epigenetic gene silencing. The screen relies on a GFP transgene that is expressed in red blood cells in a variegated manner. In the orginal transgenic FVB mice expression occurs in approximately 55% of red blood cells. During the course of my Masters, I characterised four different Mommes (Modifiers of murine metastable epiallele), MommeD32, MommeD33, MommeD35 and MommeD36. For each Momme, I identified the underlying mutation, and observed the corresponding phenotype. In MommeD32 the causative mutation is in Dnmt1, (DNA methyltransferase 1). This gene was previously identified in the screen, as MommeD2, and the new allele, MommeD32 has a change in the BAH domain of the protein. MommeD33 is the result of a change at the transgene itself. MommeD35 carries a mutation in Suv39h1 (suppressor of variegation 3-9 homolog 1). This gene has not previously been identified in the screen, but it is a known epigenetic modifier. MommeD36 had the same ENU treated sire as MommeD32, and I found that it has the same mutation as MommeD32. These mutant strains provide valuable tools that can be used to further our knowledge of epigenetic reprogramming. An example being the cancer study done with MommeD9 which has a mutation in Trim28. By crossing MommeD9+/- mutant mice with Trp53+/- mice, it can be seen if Trim28 has an effect on the rate of tumour genesis. However no clear effect of Trim28 haploinsufficiency can be observed in Trp53+/- mice.

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Aguilar, Sanchez Cristina. „Epigenetic transitions in cardiovascular development and cell reprogramming“. Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28787.

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Epigenetic modifications are alterations in the cell nucleus that affect gene expression and can occur in chromatin at the level of DNA methylation or histone modifications. Such ‘epigenetic marks’ can be heritable through cell division but leave the DNA sequence unchanged. Post-translational modifications can be found on the histone proteins associated with DNA; the majority of histone modifications are found on the lysine-rich N-‐terminal amino acid “tails”. Histone acetylation and methylation influence the chromatin structure by loosening or tightening the packaging of DNA, respectively, in association with other chromatin modifiers. Condensed chromatin is linked to transcriptional silencing and genetic imprinting and also occurs at chromosomal centromeres, where it is linked to kinetochore binding. Heart development is well studied, but the epigenetic processes involved are not yet completely understood. While active chromatin mechanisms such as histone acetylation and chromatin remodelling have been described in the heart, the role of gene repressive epigenetic mechanisms has been poorly investigated. Cardiomyocytes are post-mitotic cells that do not divide to regenerate a damaged heart. The regeneration of cardiomyocytes after myocardial infarction is an important topic of interest in cardiovascular science. There are various approaches to heart repair after infarction, including activating cardiomyocytes so they become mitotic once again, or growing cardiomyocytes in vitro to attach to a lesion site. An important factor in these approaches is understanding the epigenetic mechanisms controlling cell division. In this thesis, we aim to advance the current knowledge of the epigenetic repressive mechanisms involved in cardiomyocyte formation and heart development to explain their lack of regenerative capacities. We studied the epigenetic changes that occur during cardiac development leading to a non-‐regenerative state to pinpoint the moment at which these changes arise. We found that the epigenetic process is independent of whether cardiac lineage differentiation occurs during embryogenesis or during differentiation in vitro. We discovered that cardiac heterochromatin displays a singular epigenetic signature during development as compared to brain, another post-mitotic tissue, or liver, an actively regenerative tissue. We observed an epigenetic change in the repressive histone modification histone H3 lysine 9 trimethylation that was specific to heart development. This change involved a nuclear reorganisation of heterochromatin and a reduction of the levels of this mark in E13.5 and E14.5 embryos, as compared to E10.5 embryos. This was consistent with our observations of the histone lysine methyltransferase SUV39H1, the levels of which were lower after stage E10.5 of development. However, contradictorily, in differentiated cardiomyocytes in vitro, SUV39H1 was increased but showed low levels of H3K9me3, compared to ES cells, which had low levels of SUV39H1 and high levels of H3K9me3. We detected extremely low levels of the H3K9me3 in adult heart tissue. We observed that in adult hearts, the myocardium had maintained these major changes in H3K9me3, while this effect was not observed in the epicardium. Genomic studies were carried out to determine changes at a genomic level between the two key epigenetic stages in heart development we identified at E10.5 and E13.5. Methylated DNA immunoprecipitation sequencing and chromatin immunoprecipitation sequencing for H3K9me3 analyses were carried out to find overall changes in methylation patterns. No global changes in DNA methylation were detected between these developmental stages. These results imply that the differences observed in H3K9me3 are due to remodelling of the heterochromatin during heart development and cardiomyocyte formation, rather than quantitative changes.

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Wanichnopparat, Wachiraporn [Verfasser]. „Epigenetic reprogramming of hepatocyte-like cells / Wachiraporn Wanichnopparat“. Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2020. http://d-nb.info/1239645333/34.

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Bücher zum Thema "Epigenetic reprograming"

Meissner, Alexander, und Jörn Walter, Hrsg. Epigenetic Mechanisms in Cellular Reprogramming. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-31974-7.

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Ancelin, Katia, und Maud Borensztein, Hrsg. Epigenetic Reprogramming During Mouse Embryogenesis. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-0958-3.

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Pei, Gang, Hrsg. Epigenetic Mechanisms of Cell Programming and Reprogramming. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-7419-9.

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Meissner, Alexander, und Jörn Walter. Epigenetic Mechanisms in Cellular Reprogramming. Springer, 2015.

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Meissner, Alexander, und Jö Walter. Epigenetic Mechanisms in Cellular Reprogramming. Springer London, Limited, 2014.

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Epigenetic Mechanisms In Cellular Reprogramming. Springer-Verlag Berlin and Heidelberg GmbH &, 2014.

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Meissner, Alexander, und Jörn Walter. Epigenetic Mechanisms in Cellular Reprogramming. Springer, 2016.

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Pei, Gang. Epigenetic Mechanisms of Cell Programming and Reprogramming. Springer, 2022.

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Ancelin, Katia, und Maud Borensztein. Epigenetic Reprogramming During Mouse Embryogenesis: Methods and Protocols. Springer, 2021.

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Ancelin, Katia, und Maud Borensztein. Epigenetic Reprogramming During Mouse Embryogenesis: Methods and Protocols. Springer, 2020.

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Buchteile zum Thema "Epigenetic reprograming"

Koul, Hari K., Sankaralingam Saikolappan, Binod Kumar und Sweaty Koul. „Targeting ROS-Induced Epigenetic Reprograming in Cancer Stem Cells“. In Handbook of Oxidative Stress in Cancer: Therapeutic Aspects, 1373–86. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-5422-0_69.

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Koul, Hari K., Sankaralingam Saikolappan, Binod Kumar und Sweaty Koul. „Targeting ROS Induced Epigenetic Reprograming in Cancer Stem Cells“. In Handbook of Oxidative Stress in Cancer: Therapeutic Aspects, 1–15. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-1247-3_69-1.

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Paro, Renato, Ueli Grossniklaus, Raffaella Santoro und Anton Wutz. „Regeneration and Reprogramming“. In Introduction to Epigenetics, 135–49. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68670-3_7.

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AbstractDuring regenerative processes, cells are required to restructure parts of a damaged or worn-out organ and tissue. Here, you will become acquainted with the strategies that organisms developed to provide the material for tissue and organ repair. On the one hand, somatic cells can become dedifferentiated to increase their developmental potential and produce the plasticity required to replace the entire cellular complexity of a damaged part. On the other hand, organisms retain organ-specific stem cells with a restricted developmental potency and use these to provide the “spare parts” for replacing damaged cells. In all cases, a substantial reprogramming of the epigenome of these cells accompanies the restructuring process. In vitro strategies have been developed to drive cells back to a pluripotent state, allowing a better understanding of the underlying chromatin adjustments and providing a rich source for cellular therapies.

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Lindroth, Anders M., Yoon Jung Park und Christoph Plass. „Epigenetic Reprogramming in Cancer“. In Epigenetic Mechanisms in Cellular Reprogramming, 193–223. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-31974-7_9.

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Lin, Jer-Young, und Tzung-Fu Hsieh. „Epigenetic Reprogramming During Plant Reproduction“. In Plant Epigenetics, 405–25. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55520-1_20.

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Alberio, Ramiro, und Andrew D. Johnson. „Epigenetic Reprogramming with Oocyte Molecules“. In Nuclear Reprogramming and Stem Cells, 45–57. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-225-0_5.

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Nakamura, Toshinobu, und Toru Nakano. „Stella and Zygotic Reprogramming“. In Epigenetic Mechanisms in Cellular Reprogramming, 31–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-31974-7_2.

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Kádár, András, und Tibor A. Rauch. „Epigenetic Reprogramming in Lung Carcinomas“. In Patho-Epigenetics of Disease, 159–77. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3345-3_7.

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Schwarzer, Caroline, und Michele Boiani. „The Oocyte Determinants of Early Reprogramming“. In Epigenetic Mechanisms in Cellular Reprogramming, 1–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-31974-7_1.

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Bošković, Ana, und Maria-Elena Torres-Padilla. „Histone Variants and Reprogramming in Early Development“. In Epigenetic Mechanisms in Cellular Reprogramming, 43–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-31974-7_3.

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Konferenzberichte zum Thema "Epigenetic reprograming"

Lee, J., T. X. Pham, J. Guan, N. Caporarello, J. A. Meridew, K. M. Choi, D. Jones et al. „The Epigenetic Repressor CBX5 Drives Fibroblast Metabolic Reprograming and Lung Fibrogenesis“. In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a1144.

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Hong, J., J. Lee, T. X. Pham, J. A. Meridew, K. M. Choi, S. K. Huang, G. Lomberk, R. Urrutia und G. Ligresti. „Inhibition of the Epigenetic Regulator CBX5 Promotes Fibroblast Metabolic Reprograming and Attenuates Lung Fibrosis“. In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a2212.

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Sodre, Andressa L., David M. Woods, Amod Sarnaik, Brian C. Betts, Steven Quayle, Simon Jones und Jeffrey Weber. „Abstract 638: Epigenetic reprograming of immune cells through selective inhibition of HDAC6 reduces suppressive phenotypes and augments anti-tumor properties of T-cells“. In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-638.

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Shen, Li, Bob McGray, Anthony Miliotto, Ariel Francois, Cheryl Eppolito, Junko Matsuzaki, Takemasa Tsuji, Richard Koya und Adekunle Odunsi. „Abstract PR12: Epigenetic reprograming promotes an immunogenic ovarian tumor microenvironment and synergizes with adoptive transfer of engineered T cells expressing NY-ESO-1 specific T cell receptors“. In Abstracts: AACR Special Conference: Addressing Critical Questions in Ovarian Cancer Research and Treatment; October 1-4, 2017; Pittsburgh, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.ovca17-pr12.

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Parfenova, P. S., N. A. Mikhailova, M. G. Khotin und N. A. Kraskovskaya. „DIRECT REPROGRAMMING OF PATIENT FIBROBLAST INTO NEURON-LIKE CELLS AS A PROMISING MODEL OF HUNTINGTON’S DISEASE“. In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-111.

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The existing research of molecular mechanisms of Huntington’s disease (HD) progression, is expanded here by providing a modified method of direct reprogramming fibroblasts into neuron-like cells that keeps epigenetic changes important for late-onset HD progression. The HD cause seen as an expansion of CAG repeats within the Huntingtin gene. We anticipate our assay to be a starting point for preclinical trials on human cells rather than on mouse models.

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Shiao, Yih-Horng, W. G. Alvord, Xin Ge, Joshua M. Spurrier, Sean D. McCann, Cuiju Wang, Erik B. Crawford et al. „Abstract 184: Stress-induced father-mediated45S rRNAgenetic and epigenetic reprogramming“. In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-184.

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Benavente, Claudia A., und Michael A. Dyer. „Abstract A163: A role for epigenetic reprogramming in retinoblastoma tumorigenesis.“ In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-a163.

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Teng, Shuaishuai, Yang Li, Ming Yang, Rui Qi, Qianyu Wang, Zhi Lu und Dong Wang. „Abstract 4334: Epigenetic reprogramming of tissue-specific transcription promotes metastasis“. In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4334.

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Puca, Loredana, Dong Gao, Myriam Kossai, Joanna Cyrta, Clarisse Marotz, Juan Miguel Mosquera, Theresa Y. MacDonald et al. „Abstract B41: Targeting androgen-independent prostate cancer through epigenetic reprogramming“. In Abstracts: AACR Special Conference: Chromatin and Epigenetics in Cancer; September 24-27, 2015; Atlanta, GA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.chromepi15-b41.

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