Academic literature on the topic 'Complexe polycomb'
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Journal articles on the topic "Complexe polycomb"
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Dong, Guan-Jun, Jia-Le Xu, Yu-Ruo Qi, Zi-Qiao Yuan, and Wen Zhao. "Critical Roles of Polycomb Repressive Complexes in Transcription and Cancer." International Journal of Molecular Sciences 23, no. 17 (August 24, 2022): 9574. http://dx.doi.org/10.3390/ijms23179574.
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Polycomp group (PcG) proteins are members of highly conserved multiprotein complexes, recognized as gene transcriptional repressors during development and shown to play a role in various physiological and pathological processes. PcG proteins consist of two Polycomb repressive complexes (PRCs) with different enzymatic activities: Polycomb repressive complexes 1 (PRC1), a ubiquitin ligase, and Polycomb repressive complexes 2 (PRC2), a histone methyltransferase. Traditionally, PRCs have been described to be associated with transcriptional repression of homeotic genes, as well as gene transcription activating effects. Particularly in cancer, PRCs have been found to misregulate gene expression, not only depending on the function of the whole PRCs, but also through their separate subunits. In this review, we focused especially on the recent findings in the transcriptional regulation of PRCs, the oncogenic and tumor-suppressive roles of PcG proteins, and the research progress of inhibitors targeting PRCs.
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Strutt, H., and R. Paro. "The polycomb group protein complex of Drosophila melanogaster has different compositions at different target genes." Molecular and Cellular Biology 17, no. 12 (December 1997): 6773–83. http://dx.doi.org/10.1128/mcb.17.12.6773.
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In Drosophila the Polycomb group genes are required for the long-term maintenance of the repressed state of many developmental regulatory genes. Their gene products are thought to function in a common multimeric complex that associates with Polycomb group response elements (PREs) in target genes and regulates higher-order chromatin structure. We show that the chromodomain of Polycomb is necessary for protein-protein interactions within a Polycomb-Polyhomeotic complex. In addition, Posterior Sex Combs protein coimmunoprecipitates Polycomb and Polyhomeotic, indicating that they are members of a common multimeric protein complex. Immunoprecipitation experiments using in vivo cross-linked chromatin indicate that these three Polycomb group proteins are associated with identical regulatory elements of the selector gene engrailed in tissue culture cells. Polycomb, Polyhomeotic, and Posterior Sex Combs are, however, differentially distributed on regulatory sequences of the engrailed-related gene invected. This suggests that there may be multiple different Polycomb group protein complexes which function at different target sites. Furthermore, Polyhomeotic and Posterior Sex Combs are also associated with expressed genes. Polyhomeotic and Posterior Sex Combs may participate in a more general transcriptional mechanism that causes modulated gene repression, whereas the inclusion of Polycomb protein in the complex at PREs leads to stable silencing.
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Meseure, D., S. Vacher, M. Trassard, K. Drak Alsibai, C. Le Ray, C. Régnier, F. Lerebours, R. Le Scodan, R. Lidereau, and I. Bièche. "Rôles du complexe répresseur Polycomb EZH2/CBX7 et du long ARN non codant ANRIL dans l’induction des mécanismes de silencing épigénétique. Implications thérapeutiques potentielles dans les carcinomes mammaires de type triple négatif." Annales de Pathologie 31, no. 5 (November 2011): S125. http://dx.doi.org/10.1016/j.annpat.2011.09.021.
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Ali, Janann Y., and Welcome Bender. "Cross-Regulation among the Polycomb Group Genes in Drosophila melanogaster." Molecular and Cellular Biology 24, no. 17 (September 1, 2004): 7737–47. http://dx.doi.org/10.1128/mcb.24.17.7737-7747.2004.
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ABSTRACT Genes of the Polycomb group in Drosophila melanogaster function as long-term transcriptional repressors. A few members of the group encode proteins found in two evolutionarily conserved chromatin complexes, Polycomb repressive complex 1 (PRC1) and the ESC-E(Z) complex. The majority of the group, lacking clear biochemical functions, might be indirect regulators. The transcript levels of seven Polycomb group genes were assayed in embryos mutant for various other genes in the family. Three Polycomb group genes were identified as upstream positive regulators of the core components of PRC1. There is also negative feedback regulation of some PRC1 core components by other PRC1 genes. Finally, there is positive regulation of PRC1 components by the ESC-E(Z) complex. These multiple pathways of cross-regulation help to explain the large size of the Polycomb group family of genes, but they complicate the genetic analysis of any single member.
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Zhou, Haining, Chad B. Stein, Tiasha A. Shafiq, Gergana Shipkovenska, Marian Kalocsay, Joao A. Paulo, Jiuchun Zhang, et al. "Rixosomal RNA degradation contributes to silencing of Polycomb target genes." Nature 604, no. 7904 (March 30, 2022): 167–74. http://dx.doi.org/10.1038/s41586-022-04598-0.
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AbstractPolycomb repressive complexes 1 and 2 (PRC1 and PRC2) are histone-modifying and -binding complexes that mediate the formation of facultative heterochromatin and are required for silencing of developmental genes and maintenance of cell fate1–3. Multiple pathways of RNA decay work together to establish and maintain heterochromatin in fission yeast, including a recently identified role for a conserved RNA-degradation complex known as the rixosome or RIX1 complex4–6. Whether RNA degradation also has a role in the stability of mammalian heterochromatin remains unknown. Here we show that the rixosome contributes to silencing of many Polycomb targets in human cells. The rixosome associates with human PRC complexes and is enriched at promoters of Polycomb target genes. Depletion of either the rixosome or Polycomb results in accumulation of paused and elongating RNA polymerase at Polycomb target genes. We identify point mutations in the RING1B subunit of PRC1 that disrupt the interaction between PRC1 and the rixosome and result in diminished silencing, suggesting that direct recruitment of the rixosome to chromatin is required for silencing. Finally, we show that the RNA endonuclease and kinase activities of the rixosome and the downstream XRN2 exoribonuclease, which degrades RNAs with 5′ monophosphate groups generated by the rixosome, are required for silencing. Our findings suggest that rixosomal degradation of nascent RNA is conserved from fission yeast to human, with a primary role in RNA degradation at facultative heterochromatin in human cells.
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MA, Ke-Xue, and Xing-Zi XI. "Polycomb group protein complexes." Hereditas (Beijing) 31, no. 10 (December 22, 2009): 977–81. http://dx.doi.org/10.3724/sp.j.1005.2009.00977.
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Gahan, James M., Fabian Rentzsch, and Christine E. Schnitzler. "The genetic basis for PRC1 complex diversity emerged early in animal evolution." Proceedings of the National Academy of Sciences 117, no. 37 (August 31, 2020): 22880–89. http://dx.doi.org/10.1073/pnas.2005136117.
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Polycomb group proteins are essential regulators of developmental processes across animals. Despite their importance, studies on Polycomb are often restricted to classical model systems and, as such, little is known about the evolution of these important chromatin regulators. Here we focus on Polycomb Repressive Complex 1 (PRC1) and trace the evolution of core components of canonical and non-canonical PRC1 complexes in animals. Previous work suggested that a major expansion in the number of PRC1 complexes occurred in the vertebrate lineage. We show that the expansion of the Polycomb Group RING Finger (PCGF) protein family, an essential step for the establishment of the large diversity of PRC1 complexes found in vertebrates, predates the bilaterian–cnidarian ancestor. This means that the genetic repertoire necessary to form all major vertebrate PRC1 complexes emerged early in animal evolution, over 550 million years ago. We further show that PCGF5, a gene conserved in cnidarians and vertebrates but lost in all other studied groups, is expressed in the nervous system in the sea anemone Nematostella vectensis, similar to its mammalian counterpart. Together this work provides a framework for understanding the evolution of PRC1 complex diversity and it establishes Nematostella as a promising model system in which the functional ramifications of this diversification can be further explored.
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Chittock, Emily C., Sebastian Latwiel, Thomas C. R. Miller, and Christoph W. Müller. "Molecular architecture of polycomb repressive complexes." Biochemical Society Transactions 45, no. 1 (February 8, 2017): 193–205. http://dx.doi.org/10.1042/bst20160173.
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The polycomb group (PcG) proteins are a large and diverse family that epigenetically repress the transcription of key developmental genes. They form three broad groups of polycomb repressive complexes (PRCs) known as PRC1, PRC2 and Polycomb Repressive DeUBiquitinase, each of which modifies and/or remodels chromatin by distinct mechanisms that are tuned by having variable compositions of core and accessory subunits. Until recently, relatively little was known about how the various PcG proteins assemble to form the PRCs; however, studies by several groups have now allowed us to start piecing together the PcG puzzle. Here, we discuss some highlights of recent PcG structures and the insights they have given us into how these complexes regulate transcription through chromatin.
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Lund, Anders H., and Maarten van Lohuizen. "Polycomb complexes and silencing mechanisms." Current Opinion in Cell Biology 16, no. 3 (June 2004): 239–46. http://dx.doi.org/10.1016/j.ceb.2004.03.010.
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Schwartz, Yuri B., and Vincenzo Pirrotta. "Polycomb complexes and epigenetic states." Current Opinion in Cell Biology 20, no. 3 (June 2008): 266–73. http://dx.doi.org/10.1016/j.ceb.2008.03.002.
Full textDissertations / Theses on the topic "Complexe polycomb"
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Campagne, Antoine. "Etude du complexe Polycomb PR-DUB : une approche mécanistique." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066624/document.
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BAP1 est un suppresseur de tumeurs dont le nombre de partenaires protéiques rend complexe l'appréhension de son rôle dans la cellule. Chez la Drosophile, BAP1 et ASX forment le complexe Polycomb PR-DUB, qui déubiquitine l'histone H2A sur la lysine 119 afin de maintenir une répression transcriptionnelle sur ses gènes cibles. Comprendre les mécanismes de régulation de BAP1 et définir son implication au sein de la machinerie Polycomb s'avèrent donc des enjeux cruciaux pour mieux appréhender son rôle au cours de la tumorigenèse. Par des approches biochimiques, nous avons montré l'existence de plusieurs complexes fonctionnellement distincts associés à BAP1. ASXL1 semble ainsi nécessaire à l'activité H2A deubiquitinase de BAP1, tandis qu'ASXL2 forme un complexe ternaire avec BAP1 et la déméthylase d'histones KDM1B. Par ailleurs, nous avons démontré le potentiel de répresseur transcriptionnel de BAP1, qui semble posséder différents domaines répresseurs. Afin d'étudier ces aspects à l'échelle du génome, des analyses du transcriptome et de différentes marques d'histone sont en cours, dans des cellules sauvages ou mutées pour différents membres de la famille Polycomb. Dans un deuxième temps, nous avons entrepris une recherche exhaustive des substrats de BAP1. Nos résultats préliminaires suggèrent que non seulement H2A mais également H2B sont des cibles de BAP1, de même qu'un complexe protéique responsable du contrôle de la prolifération cellulaire via la régulation post-transcriptionnelle de plusieurs cyclines. Ces observations ouvrent la voie à plusieurs projets qui pourraient contribuer à expliquer les conséquences des mutations de BAP1 dans le processus tumoralBAP1 is as a tumor suppressor that associates to a variety of protein partners, thereby limiting the comprehension of its cellular functions. In Drosophila, BAP1 binds ASX to form the Polycomb PR-DUB complex, which deubiquitinates histone H2A on lysine 119 in order to maintain transcriptional repression on its target genes. Describing BAP1 mechanisms of action and defining how BAP1 cooperates with the Polycomb machinery are prerequisites to understand its role during tumorigenesis. Using a biochemical approach, we described the existence of several distinct subcomplexes associated with BAP1. Therefore, ASXL1 seems required for H2A deubiquitination, while ASXL2 forms a ternary complex of unknown function with BAP1 and the histone demethylase KDM1B. In addition, we demonstrated the transcriptional repressor function of BAP1, which possess several repressive domains. In addition, we are currently performing transcriptomic analysis combined with genome-wide mapping of different histone marks. These last analyses are performed in wild type cells or deficient in PR-DUB or other Polycomb components, which will help us to understand how BAP1 fits within the Polycomb machinery. In parallel, we engaged a comprehensive study aiming at the identification of new BAP1 substrates. Our preliminary results suggest that not only H2A but also H2B may be direct substrates of BAP1. In addition, we identified as a potential substrate the HNRNPM-IMP3 complex, which controls cell proliferation via post-transcriptional regulation of several cyclins. These observations pave the way for new projects that may contribute to explain the consequences of BAP1 mutations in cancer development
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Campagne, Antoine. "Etude du complexe Polycomb PR-DUB : une approche mécanistique." Electronic Thesis or Diss., Paris 6, 2015. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2015PA066624.pdf.
Full textAbstract:
BAP1 est un suppresseur de tumeurs dont le nombre de partenaires protéiques rend complexe l'appréhension de son rôle dans la cellule. Chez la Drosophile, BAP1 et ASX forment le complexe Polycomb PR-DUB, qui déubiquitine l'histone H2A sur la lysine 119 afin de maintenir une répression transcriptionnelle sur ses gènes cibles. Comprendre les mécanismes de régulation de BAP1 et définir son implication au sein de la machinerie Polycomb s'avèrent donc des enjeux cruciaux pour mieux appréhender son rôle au cours de la tumorigenèse. Par des approches biochimiques, nous avons montré l'existence de plusieurs complexes fonctionnellement distincts associés à BAP1. ASXL1 semble ainsi nécessaire à l'activité H2A deubiquitinase de BAP1, tandis qu'ASXL2 forme un complexe ternaire avec BAP1 et la déméthylase d'histones KDM1B. Par ailleurs, nous avons démontré le potentiel de répresseur transcriptionnel de BAP1, qui semble posséder différents domaines répresseurs. Afin d'étudier ces aspects à l'échelle du génome, des analyses du transcriptome et de différentes marques d'histone sont en cours, dans des cellules sauvages ou mutées pour différents membres de la famille Polycomb. Dans un deuxième temps, nous avons entrepris une recherche exhaustive des substrats de BAP1. Nos résultats préliminaires suggèrent que non seulement H2A mais également H2B sont des cibles de BAP1, de même qu'un complexe protéique responsable du contrôle de la prolifération cellulaire via la régulation post-transcriptionnelle de plusieurs cyclines. Ces observations ouvrent la voie à plusieurs projets qui pourraient contribuer à expliquer les conséquences des mutations de BAP1 dans le processus tumoralBAP1 is as a tumor suppressor that associates to a variety of protein partners, thereby limiting the comprehension of its cellular functions. In Drosophila, BAP1 binds ASX to form the Polycomb PR-DUB complex, which deubiquitinates histone H2A on lysine 119 in order to maintain transcriptional repression on its target genes. Describing BAP1 mechanisms of action and defining how BAP1 cooperates with the Polycomb machinery are prerequisites to understand its role during tumorigenesis. Using a biochemical approach, we described the existence of several distinct subcomplexes associated with BAP1. Therefore, ASXL1 seems required for H2A deubiquitination, while ASXL2 forms a ternary complex of unknown function with BAP1 and the histone demethylase KDM1B. In addition, we demonstrated the transcriptional repressor function of BAP1, which possess several repressive domains. In addition, we are currently performing transcriptomic analysis combined with genome-wide mapping of different histone marks. These last analyses are performed in wild type cells or deficient in PR-DUB or other Polycomb components, which will help us to understand how BAP1 fits within the Polycomb machinery. In parallel, we engaged a comprehensive study aiming at the identification of new BAP1 substrates. Our preliminary results suggest that not only H2A but also H2B may be direct substrates of BAP1. In addition, we identified as a potential substrate the HNRNPM-IMP3 complex, which controls cell proliferation via post-transcriptional regulation of several cyclins. These observations pave the way for new projects that may contribute to explain the consequences of BAP1 mutations in cancer development
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Molitor, Anne. "Caractérisation moléculaire et fonctionnelle du complexe PRC1 chez Arabidopsis thaliana." Thesis, Strasbourg, 2012. http://www.theses.fr/2012STRAJ053.
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Les protéines du groupe Polycomb sont des régulateurs épigénétiques impliqués dans divers processus développementaux et cellulaires. Le complexe Polycomb Répressif 1 (PRC1) est bien caractérisé chez les animaux, cependant sa composition et sa fonction restent énigmatiques dans les plantes. Sur base d'homologie de séquences trois homologues de la sous-unité de base BMI1 du complexe PRC1 animal ont été identifiés dans Arabidopsis: AtBMI1a, AtBMI1b et AtBMI1c. L'interaction de ces trois protéines avec les composantes PRC1 connues (i.e. AtRING1ab, et LHP1) a été démontrée. Des analyses génétiques et moléculaires ont permis d'attribuer aux protéines AtBMI1ab et AtRING1ab un rôle essentiel dans la répression des caractères embryonnaire lors de la croissance végétative. Un nouvel interactant d'AtRING1a, une protéine à domaine PHD de la famille AL (Alfine-Like) a été identifiée dans criblage d'une banque de ADNc. Par différentes techniques l'association entre les protéines de la famille AL et les membres de bases du complexe PRC1 (i.e. AtBMI1ab, AtRING1ab et LHP1) a été démontrée. Les protéines AL sont nucléaires et se lient in vitro à H3k4me3, une marque active de la chromatine. Des analyses génétiques ont révélé que les protéines AL et AtBMI1ab régulent la germination en réprimant l'expression de gènes impliqués dans le développement de la graine. Au niveau chromatinien, les protéines PRC1 interviennent dans la transition d'une chromatine active, marquée par du H3K4me3 vers une chromatine répressive enrichie en H3K27me3. Nous proposons que les protéines AL reconnaissent la marque active et recrutent la fonction répressive des protéines à domaine RING du complexe PRC1 afin d'induire la répression transcriptionellePolycomb group (PcG) proteins are critical epigenetic repressors implicated in various developmental and cellular processes. While the Polycomb Repressive Complex 2 (PRC2) is evolutionary conserved and its functions extensively studied in Arabidopsis, the PRC1 complex composition and function remain still enigmatic in plants. Our work focuses on several Arabidopsis RING-domain proteins to unravel PRC1-like functions in the regulation of various processes during plant development. Based on sequence similarity we identified three homologues of the animal PRC1 core subunit BMI1: AtBMI1a, AtBMI1b and AtBMI1c. These proteins were found to interact with other PRC1-like components, AtRING1a, AtRING1b and LHP1. Genetic and molecular analyses demonstrated that AtBMI1a/b and AtRING1a/b play crucial roles in stable repression of embryonic traits to allow proper somatic growth. Comparative transcriptome analyses were performed to uncover genetic networks underlying seedling growth and the flower development defects of several different PRC1-like and PRC2 Arabidopsis mutants. Our data revealed overlapping and non-overlapping gene categories of misregulated genes in Atring1a/b, Atbmi1a/b and lhp1 mutants. The Atring1a/b mutant showed particular disturbed expression of flower developmental genes. Accordingly, phenotypic and molecular analyses of the mutant flowers confirmed that AtRING1a/b play a critical role in cell fate determination and in different aspects of flower development. To better understand the broad function of AtRING1a/b, we performed yeast two-hybrid screen and identified PHD-domain proteins of the ALFIN-LIKE (AL) family as binding partners. In vitro AL proteins bind the active mark for gene transcription, H3K4me3. By various methods, both in vitro and in planta, we provided strong evidence for the physical interaction between AL and PRC1 RING-domain proteins. We uncovered that al6/7 similar to Atbmi1a/b mutants exhibit seed germination defects, which are associated with the derepression of several seed related genes. Consistently on the corresponding chromatin a delay of the remodeling from active H3K4me3 labeled to a repressive H3K27me3 marked chromatin could be detected. We propose that through binding to H3K4me3 AL6/7 function as scaffold proteins to target PRC1 RING-domain proteins to active chromatin in order to establish gene silencing. Taken together, the presented work contributes significantly to the knowledge of PRC1 complex(es) in Arabidopsis at both biological function and complex composition levels. It opens several exciting perspectives for future research in the field
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Netter, Sophie. "Identification d'un nouveau complexe de genes a homeoboite cible des proteines des groupes polycomb et trithorax : le complexe iroquois." Paris 6, 1998. http://www.theses.fr/1998PA066258.
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J'ai caracterise des insertions de genes rapporteurs w presentant un profil d'expression differentiel sur l'axe dorso-ventral (d/v) dans l'il de drosophile. Ce profil est stable et hereditaire. Cette etude m'a permis d'isoler des genes impliques dans des processus regulateurs du developpement. J'ai montre que tous les transgenes presentant un profil d/v etaient localises dans une region unique du genome s'etendant sur 140 kb au niveau du site 69d, decrit comme etant un site de fixation de plusieurs proteines du pc-g. Cette region contient au moins trois genes, araucan (ara), caupolican (caup) et mirror (mirr), qui codent des proteines a homeodomaine tres similaires et constituent le complexe iroquois (iro-c). Ces genes sont impliques dans des processus developpementaux communs, mais semblent egalement avoir des fonctions specifiques, notamment dans la mise en place de la polarite dorso-ventrale de l'embryon et le developpement de l'aile. J'ai montre que l'expression de ces trois genes dans l'il est controlee par les produits des genes des groupes polycomb (pc-g) et trithorax (trx-g). Le produit du gene polyhomeotic est requis pour maintenir la repression de l'expression de mirr dans la moitie ventrale du disque imaginal d'il au stade larvaire, mais pas dans les autres tissus larvaires, ni au cours de l'embryogenese. Enfin, j'ai etudie le role des genes du iro-c dans la formation des soies sensorielles du thorax et dans le developpement de l'aile. Ainsi, j'ai pu identifier un nouveau complexe de genes a homeoboite, cible des produits des genes du pc-g et du trx-g. L'ensemble des travaux presentes sur ce complexe indique que ces genes jouent un role central au cours du developpement embryonnaire et post-embryonnaire. Je propose que le maintien de la repression des genes du iro-c dans l'il serait mediee par un mecanisme de compaction locale de la structure de la chromatine impliquant les proteines du pc-g.
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Cedrone, L. "THE ROLE OF ENHANCED POLYCOMB REPRESSIVE COMPLEX 2 ACTIVITY IN TUMORIGENESIS." Doctoral thesis, Università degli Studi di Milano, 2017. http://hdl.handle.net/2434/468289.
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Polycomb Group of proteins are essential factors present in cells’ nuclei. These multiprotein complexes are key repressive chromatin factors that regulate cellular differentiation during development, contributing to the correct establishment of lineage-specific transcriptional programs. Moreover, they represent key factors of proliferation and deregulation of their levels and activity have been linked to the onset and development of several human cancers.
Recently, gain of function heterozygous EZH2 mutations have been discovered in non-Hodgkin lymphomas and melanomas. These mutations cause an aminoacidic substitution within the EZH2 catalytic SET domain (Y641), resulting in increased H3K27me3 deposition. Very little is known about this mutated enzyme, therefore the aim of my thesis is trying to unravel the tumorigenic mechanisms underlying these mutations. To understand a general oncogenic role for this mutated enzyme, we used MEF as an alternative, simpler model system. We observed increased deposition of H3K27me3 without any relevant transcriptional alteration at steady state, confirming our results also in lymphoma cell lines. To investigate a cooperative transcriptional deregulation for mutant EZH2, we then subjected MEFs to three different stimuli (starvation, myc upregulation and reprogramming to pluripotency). Since we found this to be true only during cell-fate transition, we proposed a model in which the levels of the H3K27me3 are increasingly deposited where the mark is already present at steady state. This could be relevant in lymphomas, impeding centroblasts differentiation and resulting in tumorigenesis in the presence of concomitant oncogenic mutations. This observation could shed light on the molecular mechanisms underlying lymphomagenesis in patients.
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Jacobs, Chean Sern. "Role of PRC2-mediated chromatin regulation in fine tuning Arabidopsis root development." Thesis, Lyon, 2020. http://www.theses.fr/2020LYSEN085.
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La régulation de l’expression des gènes par la voie des mécanismes chromatiniennes sont critiques dans la modulation et la stabilisation de l’expression des programmes génétiques, essentielles pour l’organogenèse et le développement. Le complexe répresseur Polycomb 2 (PRC2) catalyse le triple méthylation de la lysine 27 de l’histone H3 auprès des gènes cibles. Ceci est un régulateur des programmes du développement, globalement conservé chez les eucaryotes multicellulaires. Afin de déterminer l’implication de PRC2 au cours des transitions de l’identité cellulaire, j’ai caractérisé le paysage chromatinien d’un type cellulaire unique de la niche des cellules souches racinaire. L’intégration quantitative des données épigénomique a révélé trois types chromatiniens qui corrèlent avec des niveaux d’activité transcriptionnelle, ainsi que des profils d’expression bien distincts, au cours de la différentiation cellulaire. Ces données suggèrent que la régulation par PRC2 est importante pour maintenir le contrôle temporel des gènes pendant l’avancé de la différentiation cellulaire. De plus, j’ai effectué des études fonctionnelles sur deux homologues de la sous unité catalytique de PRC2 qui indique que au moins deux complexes PRC2 de composition diffèrent peuvent coopérer afin de moduler finement la régulation des gènes clés du développement. En conclusion, le travail mené souligne l’importance de PRC2 dans le contrôle précis des profils d’expression des gènes, et aussi la capacité des données épigénétique d’un état précoce de différentiation de prédire l’activité transcriptionnelle dans les étapes plus tardivesChromatin-based mechanisms are pivotal regulators of transcriptional patterns that are central to cell fate determination, organogenesis and development in multicellular organisms. The activity of Polycomb Repressive Complex 2 (PRC2) is involved in the maintenance of transcriptional gene repression by catalysing the trimethylation of histone H3 on lysine 27 at specific loci, and is a conserved modulator of developmental programs.To reveal the extent to which PRC2 shapes transcriptional decisions during cell fate specification, I have characterized the epigenome organization of a single cell type from the root stem cell niche (SCN). Quantitative integration of (epi)-genomic data revealed three main chromatin states that correlate with distinct gene expression levels as well as patterns along the differentiation gradient. These results indicate that PRC2 activity over specific genes within the SCN regulates their timing of expression in daughter cells, at successive differentiation stages.In addition, functional studies of PRC2 catalytic subunit homologues support the notion that distinct PRC2 complexes with different compositions cooperate to fine-tune the transcriptional regulation of key regulatory genes during root development. Taken together, this work highlights the importance of PRC2-regulated chromatin states in shaping expression patterns along a differentiation gradient. They also pinpoint the potential of such epigenetic studies in predicting, from an initial chromatin state, the timing of gene transcriptional activation in subsequent differentiation stages
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LA, MASTRA FEDERICA. "POLYCOMB GROUP PROTEINS RING1A/RING1B CONTROL PERIPHERAL B CELL HOMEOSTASIS AND TERMINAL DIFFERENTIATION." Doctoral thesis, Università degli Studi di Milano, 2019. http://hdl.handle.net/2434/609574.
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Polycomb Repressive Complex 1 and 2 (PRC1 and PRC2) modulate chromatin accessibility through covalent histone modifications. The ubiquitous expression of PRC1 catalytic subunits throughout B cell development hypothesized roles for PRC1 in B cell physiology. This study aimed to dissect the contribution of PRC1 to peripheral B cell maturation, homeostasis and terminal differentiation. We analyzed mutant mice allowing conditional Cre-dependent inactivation of PRC1 catalytic function starting from late transitional B cells. In response to induced PRC1 inactivation, peripheral B cells in secondary lymphoid organs were reduced in number and displayed alterations in the surface phenotype, which reflected a major disturbance of their transcriptional profile. Reduced fitness of PRC1 mutant resting B cells was associated to heightened sensitivity to pro-apoptotic signals, consequent of the higher levels in these cells of the BIM protein and of the sub-optimal activation of the AKT kinase in response to either BAFF-R or BCR engagement. PRC1 mutant mice displayed major defects in the marginal zone (MZ) B cell subset, both in number and localization. This phenotype correlated with reduced expression of the Sphingosine-1-phosphate receptor-1 (S1pr1), which is crucial for B cell migration to the MZ, and the increased expression of the Polycomb target microRNA mir-125b, which targets S1pr1 transcript. Moreover, PRC1 mutant B cells displayed premature de-repression of Prdm1 gene and facilitated plasma cell differentiation upon lipopolysaccharide stimulation. Our work provides evidence for a crucial role played by PRC1 in peripheral B cell subset differentiation, B cell homeostasis and timing of terminal B cell differentiation.
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Brule, Baptiste. "Caractérisation et modulation non pharmacologique des dérégulations épigénétiques associées à la maladie de Huntington : vers l’identification de nouvelles cibles thérapeutiques." Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ015.
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La maladie de Huntington (MH) est une maladie neurodégénérative génétique caractérisée par des symptômes moteurs, cognitifs et psychiatriques causés par une atteinte primaire du striatum. Le mécanisme pathogénique implique une dérégulation épigénétique et transcriptionnelle à l’origine d’une perte d’identité et de fonction des neurones. Cette thèse a consisté en la caractérisation épigénétique du striatum de modèles murins à une résolution type cellulaire-spécifique et à différent stades de la MH. Nous avons observé que les neurones striataux qui expriment le gène muté dans la MH présentent une érosion épigénétique traduisant un vieillissement accéléré qui implique une altération des complexes polycomb. Les régulations épigénétiques étant sensibles à l’environnement, nous avons caractérisé le phénotype comportemental et moléculaire de modèles murins de la MH hébergés en environnement enrichi (EE) afin de décrypter l’effet de l’EE sur les régulations épigénétiques et transcriptionnelles. Nos résultats permettent une meilleure compréhension des mécanismes pathogéniques de la MH, et offrent de nouvelles perspectives thérapeutiquesHuntington's disease (HD) is a neurodegenerative genetic disease characterized by motor, cognitive, and psychiatric disorders caused by primary damage to the striatum. The pathogenic mechanism is complex and involve epigenetic and transcriptional dysregulations leading to a loss of neuronal identity and cell function. This thesis aimed to characterize the striatal epigenetic signature in mouse models with a celltype-specific resolution at different stages of HD. We observed that striatal neurons expressing the HD mutation undergo epigenetic erosion, reflecting accelerated aging in HD, induced by alterations in polycomb complexes. As epigenetic regulations are sensitive to the environment, we characterized the behavioral phenotype and molecular alterations of HD mouse model after housing in an enriched environment (EE) to decipher the epigenetic and transcriptomic effects induced by EE. Our findings thus provide a better understanding of early pathogenic mechanisms in HD, opening new therapeutic perspectives
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Schivre, Geoffrey. "Transcriptome augmentation, Polycomb-mediated chromatin dynamics and their links to metabolism during Arabidopsis thaliana photomorphogenesis." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASB014.
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La lumière permet aux plantes de métaboliser le carbone atmosphérique grâce à la photosynthèse, constituant ainsi leur source d'énergie. Par ailleurs, les différentes propriétés de la lumière constituent une source d'informations essentielles sur leur environnement perçues par de multiples capteurs de lumière, les photorécepteurs, déclenchant des réponses adaptatives spécifiques. Parmi elles, l'une des adaptations développementales les plus spectaculaires des plantes, appelée photomorphogenèse, se produit lorsqu'une jeune plantule en cours de germination est exposée à la lumière pour la première fois. Les plantules germant sous terre, à l'abri de la lumière, suivent un développement étiolé ou skotomorphogénique, au cours duquel l'allongement rapide de l'hypocotyle facilite l'émergence de la plante à la surface, tandis que la maturation des cotylédons et la mise en place de la photosynthèse sont inhibés. La croissance skotomorphogénique repose donc entièrement sur les réserves métaboliques principalement stockées dans les cotylédons. Lorsque la surface du sol est atteinte, la détection de la lumière par les photorécepteurs déclenche l'expansion, sans division cellulaire, des cotylédons et la biogenèse des chloroplastes permettant l'acquisition de la photo-autotrophie. Au niveau moléculaire, le dé-étiolement des cotylédons est associé à une spécialisation du transcriptome et à une intensification de l'activité de l'ARN polymérase II (ARN Pol II). A l'échelle cytologique, de profonds réarrangements de la chromatine conduisent à l'élargissement du noyau et à la condensation des régions péricentromériques au sein de foyers hétérochromatiniens. Considérant qu'une grande partie de ces contrôles métaboliques, cellulaires, moléculaires et cytologiques sont réalisés de manière synchrone au cours de la transition, la photomorphogenèse d'A. thaliana constitue un modèle de choix pour caractériser les interactions entre la signalisation lumière, la régulation des gènes et les dynamiques chromatiniennes avec le statut énergétique de la plante. Au cours de ma thèse, j'ai développé une analyse de données de séquençage ARN normalisées grâce à une référence exogène pour revisiter les connaissances actuelles sur les changements transcriptomiques au vu de l'augmentation globale de l'activité de l'ARN Pol II. Ceci a permis d'identifier un doublement de l'abondance des transcrits pendant la photomorphogenèse des cotylédons qui résulte très probablement de l'augmentation de l'activité de l'ARN Pol II. J'ai ensuite exploré le rôle joué par le senseur métabolique Target Of Rapamycin (TOR) dans la régulation du régime transcriptionnel ainsi que dans la composition et l'organisation de la chromatine lors du dé-étiolement des cotylédons. Cette seconde partie de mon étude apporte un nouvel éclairage sur les liens fonctionnels entre la voie TOR et l'homéostasie d'une marque d'histone, la triméthylation de la lysine 27 de l'histone H3 (H3K27me3), catalysée par le complexe Polycomb Repressive Complexe 2 (PRC2). En particulier, elle révèle que H3K27me3 est moins abondant dans la chromatine des cotylédons étiolés que dans celle des cotylédons photomorphogéniques, un effet général qui s'avère sensible au sucre et à la signalisation TOR. Par conséquent, ces travaux mettent en évidence des rôles inattendus de la signalisation TOR et de la marque H3K27me3 dans la régulation du régime transcriptionnel général et ouvrent de nouvelles perspectives sur la régulation transcriptionnelle régie par TOR. De futures études visant à décrypter le rôle de l'homéostasie de H3K27me3, en particulier sur les gènes de réponse à la lumière, devraient permettre de mieux comprendre comment la signalisation métabolique interagit avec les dynamiques de l'épigénome et la répression transcriptionnelle régies par PRC2 avec des implications au-delà de la photomorphogenèse des plantesLight fuels plant photosynthesis providing the energy source for growth. Light intensity and quality also convey essential information on the plant's immediate surroundings, which are integrated through multiple light sensors, the photoreceptors, enabling developmental and physiological adaptations. The photomorphogenic transition, or de-etiolation, occurs when a young germinating plantlet is exposed to light for the first time, and is one of the most spectacular plant developmental adaptations to light. Seedlings germinating underground, protected from light, undergo an etiolated development, or skotomorphogenesis, during which rapid hypocotyl elongation facilitates plant drilling through the soil, while cotyledon maturation is arrested and the plantlet remains non-photosynthetic. In the absence of photosynthesis, skotomorphogenic growth relies entirely on the plant metabolic reserves, predominantly stored in cotyledons. Upon reaching the soil surface, photoreceptor light sensing triggers the expansion and greening of cotyledons, independently from cell divisions. Inducing chloroplast biogenesis and the acquisition of photosynthesis, this developmental switch marks the transition toward photo-autotrophy. At the molecular scale, cotyledon de-etiolation associates with a specialization of the transcriptome and an intensification of RNA polymerase II (RNA Pol II) activity. At the cytological scale, chromatin rearrangements lead to nucleus enlargement and the condensation of pericentromeric regions in conspicuous heterochromatic foci. Considering that much of these metabolic, cellular, molecular and cytological controls are synchronously achieved during the transition, A. thaliana photomorphogenesis is a model of choice to characterize the interplays between light signaling, gene regulation and chromatin dynamics as well as their link to the plant energetic status. During my thesis, I first contributed to develop an RNA-seq normalization methodology to revisit transcriptome changes in light of the global increase in RNA Pol II activity. This identified a 2-fold increase in transcript abundance during cotyledon photomorphogenesis, which most likely results from the increase in RNA Pol II activity. I further explored the role played by the conserved metabolic sensor Target Of Rapamycin (TOR) in defining the transcriptional regime along with chromatin composition and organization during cotyledon photomorphogenesis. This notably shed a new light on the functional links between the TOR pathway and the homeostasis of a specific histone mark, trimethylation of histone H3 at lysine 27 (H3K27me3), mediated by Polycomb Repressive Complex 2 (PRC2). More precisely, this study revealed that H3K27me3 is less abundant at chromatin in etiolated cotyledons as compared to photomorphogenic ones, a global effect that was further shown here to be sensitive to sugar and TOR signaling. Hence, this work points towards unexpected roles of TOR signaling and the PRC2-regulated mark H3K27me3 in the global regulation of transcription and opens new perspectives on TOR-mediated gene regulation. Future studies aimed at deciphering the role of H3K27me3 homeostasis, especially at specific genes induced by light, should provide new insight on how metabolic signaling interplays with Polycomb-mediated chromatin dynamics and transcription with implications beyond plant photomorphogenesis
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Lamiable, Olivier. "Identification et caractérisation des partenaires protéiques de DSP1 chez Drosophila melanogaster." Phd thesis, Université d'Orléans, 2010. http://tel.archives-ouvertes.fr/tel-00558801.
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Chez les eucaryotes pluricellulaires, la différenciation des cellules repose en partie sur l'activation oula répression des gènes. Les profils d'expression génique mis en place vont perdurer d'une générationcellulaire à l'autre. Ce phénomène met en jeu des mécanismes épigénétiques qui remodèlentlocalement la structure de la chromatine. Chez Drosophila melanogaster, les protéines des groupesPolycomb (PcG) et Trithorax (TrxG) participent au maintien du profil d'expression des gènes au coursdu développement. Les protéines PcG maintiennent les gènes réprimés tandis que les protéines TrxGmaintiennent les gènes activés. Une troisième classe de protéines nommée Enhancers of Trithoraxand Polycomb (ETP) module l'activité des PcG et TrxG. Dorsal Switch Protein 1 (DSP1) est uneprotéine HMGB (High Mobility Group B) classée comme une ETP. Par tamisage moléculaire, nousavions montré que la protéine DSP1 était présente au sein de complexes de poids moléculaire de 100kDa à 1 MDa. Le travail de thèse présenté ici a pour but d'identifier les partenaires de la protéineDSP1 dans l'embryon et de mieux connaître les propriétés biochimiques de DSP1. Premièrement, j'aimis en place puis effectué l'immunopurification des complexes contenant DSP1 dans des extraitsprotéiques embryonnaires. Cette approche nous a permis d'identifier 23 partenaires putatifs de laprotéine DSP1. Parmi ces protéines, nous avons identifié la protéine Rm62 qui est une ARN hélicaseà boîte DEAD. Les relations biologiques entre DSP1 et Rm62 ont été précisées. Deuxièmement, j'aidéterminé, par une approche biochimique, de nouvelles caractéristiques physico-chimiques de laprotéine DSP1.
Books on the topic "Complexe polycomb"
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Coleman, Rory Tristan. Making Memories: Modes and Mechanisms of Gene Silencing by the Polycomb Repressive Complexes in Drosophila. [New York, N.Y.?]: [publisher not identified], 2017.
Find full textBook chapters on the topic "Complexe polycomb"
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Brahmachari, Vani, and Shruti Jain. "Polycomb Complexes." In Encyclopedia of Systems Biology, 1720. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_854.
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Palacios, Daniela. "The Dynamics of Polycomb Complexes." In Methods in Molecular Biology, 139–42. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6380-5_12.
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Guo, Yiran, Yao Yu, and Gang Greg Wang. "Polycomb Repressive Complex 2 in Oncology." In Cancer Treatment and Research, 273–320. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-45654-1_9.
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Duarte-Aké, Fátima, Geovanny Nic-Can, and Clelia De-la-Peña. "Somatic Embryogenesis: Polycomb Complexes Control Cell-to-Embryo Transition." In Epigenetics in Plants of Agronomic Importance: Fundamentals and Applications, 339–54. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-14760-0_13.
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Vidal, Miguel. "Polycomb Complexes: Chromatin Regulators Required for Cell Diversity and Tissue Homeostasis." In Transcriptional and Epigenetic Mechanisms Regulating Normal and Aberrant Blood Cell Development, 95–139. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-45198-0_5.
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Liu, Xin. "A Structural Perspective on Gene Repression by Polycomb Repressive Complex 2." In Subcellular Biochemistry, 519–62. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-58971-4_17.
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Paro, Renato, Ueli Grossniklaus, Raffaella Santoro, and Anton Wutz. "Cellular Memory." In Introduction to Epigenetics, 49–66. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68670-3_3.
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AbstractThe identity of cells in an organism is largely defined by their specific transcriptional profile. During cell division, these profiles need to be faithfully inherited to the daughter cells to ensure the maintenance of cell structure and function in a cell lineage. Here, you will learn how two groups of chromatin regulators, the Polycomb group (PcG) and the Trithorax group (TrxG), act in an antagonistic manner to maintain differential gene expression states. Members of the PcG cooperate in large multiprotein complexes to modify histones with repressive marks, resulting in condensed chromatin domains. Conversely, the TrxG proteins counteract the repressed domains by opening nucleosomal structures and establishing activating histone modifications. PcG and TrxG proteins are evolutionary highly conserved and control diverse processes, such as the identity of stem cells in mammalian development to the process of vernalization in plants.
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Shirai, Manabu, Yoshihiro Takihara, and Takayuki Morisaki. "Pcgf5 Contributes to PRC1 (Polycomb Repressive Complex 1) in Developing Cardiac Cells." In Etiology and Morphogenesis of Congenital Heart Disease, 305–12. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-54628-3_43.
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Luo, Ming, Mingzhu Luo, Fred Berger, E. S. Dennis, Jim W. Peacock, and Abed Chaudhury. "DNA-METHYLTRANSFERASE 1 is a Member of FIS Polycomb Complex and is Involved in Seed Development in Arabidopsis." In Biotechnology and Sustainable Agriculture 2006 and Beyond, 131–33. Dordrecht: Springer Netherlands, 2007. http://dx.doi.org/10.1007/978-1-4020-6635-1_16.
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Pirrotta, V. "Global Functions of PRC2 Complexes." In Polycomb Group Proteins, 317–48. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-12-809737-3.00013-1.
Full textConference papers on the topic "Complexe polycomb"
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Iwata, Shintaro. "Abstract 4898: Polycomb group molecule PHC3 regulates polycomb complex composition and prognosis of osteosarcoma." 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.am10-4898.
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Cao, Qi, Ram Mani, Bushra Ateeq, Saravana M. Dhanasekaren, Irfan Asangani, Jindan Yu, John Prensner, et al. "Abstract 2795: An onco-protein axis linking polycomb repressive complex 2 and polycomb repressive complex 1 through miRNAs in cancer." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2795.
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Wilson, Boris G., Xi Wang, Xiaohua Shen, Elizabeth S. McKenna, Madeleine E. Lemieux, Yoon-Jae Cho, Edward C. Koelhoffer, Scott L. Pomeroy, Stuart H. Orkin, and Charles W. M. Roberts. "Abstract LB-237: Epigenetic antagonism between Polycomb and SWI/SNF complexes duringoncogenic transformation." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-lb-237.
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Wilson, Boris G., Xiaohua Shen, Elizabeth S. McKenna, Xi Wang, Yoon-Jae Cho, Edward C. Koellhoffer, Phuong T. L. Nguyen, Scott L. Pomeroy, Stuart H. Orkin, and Charles W. M. Roberts. "Abstract 4799: Epigenetic antagonism between Polycomb and SWI/SNF complexes during oncogenic transformation." 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.am10-4799.
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ZHU, Junyu, Lili Li, Connie W. Hui, Joanna H. Tong, Raymond Chan, Chi Hang Wong, Qiyong Ai, et al. "Abstract 2923: Targeting the polycomb repressive complex-2 related proteins in nasopharyngeal carcinoma." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2923.
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Chen, Fan, and Christine F. Brainson. "Abstract 5189: Activity of polycomb repressive complex 2 determines sensitivity to epigenetic therapy." 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.sabcs18-5189.
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Chen, Fan, and Christine F. Brainson. "Abstract 5189: Activity of polycomb repressive complex 2 determines sensitivity to epigenetic therapy." 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.am2019-5189.
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Cao, Qi, Xiaoju Wang, Meng Zhao, Rendong Yang, Rohit Malik, Yuanyuan Qiao, Anton Poliakov, et al. "Abstract LB-132: The central role of EED in orchestration of polycomb group complexes." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-lb-132.
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Li, Yajun, Beth O. Van Emburgh, Bilian Jin, and Keith D. Robertson. "Abstract 4868: Interaction between DNMT3B and polycomb repression complexes and their role in histone modification." 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.am10-4868.
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Junco, Sarah E., Vivian J. Bardwell, Chongwoo A. Kim, Renjing Wang, Angela Robinson, Udayar Ilangovan, Alex Taylor, et al. "Abstract C28: Binding to BCOR defines a subfamily of Psc ortholog mediated polycomb group complexes." In Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-c28.
Full textReports on the topic "Complexe polycomb"
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Ohad, Nir, and Robert Fischer. Regulation of plant development by polycomb group proteins. United States Department of Agriculture, January 2008. http://dx.doi.org/10.32747/2008.7695858.bard.
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Our genetic and molecular studies have indicated that FIE a WD-repeat Polycomb group (PcG) protein takes part in multi-component protein complexes. We have shown that FIE PcG protein represses inappropriate programs of development during the reproductive and vegetative phases of the Arabidopsis life cycle. Moreover, we have shown that FIE represses the expression of key regulatory genes that promote flowering (AG and LFY), embryogenesis (LEC1), and shoot formation (KNAT1). These results suggest that the FIE PcG protein participates in the formation of distinct PcG complexes that repress inappropriate gene expression at different stages of plant development. PcG complexes modulate chromatin compactness by modifying histones and thereby regulate gene expression and imprinting. The main goals of our original project were to elucidate the biological functions of PcG proteins, and to understand the molecular mechanisms used by FIE PcG complexes to repress the expression of its gene targets. Our results show that the PcG complex acts within the central cell of the female gametophyte to maintain silencing of MEA paternal allele. Further more we uncovered a novel example of self-imprinting mechanism by the PgG complex. Based on results obtained in the cures of our research program we extended our proposed goals and elucidated the role of DME in regulating plant gene imprinting. We discovered that in addition to MEA,DME also imprints two other genes, FWA and FIS2. Activation of FWA and FIS2 coincides with a reduction in 5-methylcytosine in their respective promoters. Since endosperm is a terminally differentiated tissue, the methylation status in the FWA and FIS2 promoters does not need to be reestablished in the following generation. We proposed a “One-Way Control” model to highlight differences between plant and animal genomic imprinting. Thus we conclude that DEMETER is a master regulator of plant gene imprinting. Future studies of DME function will elucidate its role in processes and disease where DNA methylation has a key regulatory role both in plants and animals. Such information will provide valuable insight into developing novel strategies to control and improve agricultural traits and overcome particular human diseases.
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Ohad, Nir, and Robert Fischer. Regulation of Fertilization-Independent Endosperm Development by Polycomb Proteins. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7695869.bard.
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Arabidopsis mutants that we have isolated, encode for fertilization-independent endosperm (fie), fertilization-independent seed2 (fis2) and medea (mea) genes, act in the female gametophyte and allow endosperm to develop without fertilization when mutated. We cloned the FIE and MEA genes and showed that they encode WD and SET domain polycomb (Pc G) proteins, respectively. Homologous proteins of FIE and MEA in other organisms are known to regulate gene transcription by modulating chromatin structure. Based on our results, we proposed a model whereby both FIE and MEA interact to suppress transcription of regulatory genes. These genes are transcribed only at proper developmental stages, as in the central cell of the female gametophyte after fertilization, thus activating endosperm development. To test our model, the following questions were addressed: What is the Composition and Function of the Polycomb Complex? Molecular, biochemical, genetic and genomic approaches were offered to identify members of the complex, analyze their interactions, and understand their function. What is the Temporal and Spatial Pattern of Polycomb Proteins Accumulation? The use of transgenic plants expressing tagged FIE and MEA polypeptides as well as specific antibodies were proposed to localize the endogenous polycomb complex. How is Polycomb Protein Activity Controlled? To understand the molecular mechanism controlling the accumulation of FIE protein, transgenic plants as well as molecular approaches were proposed to determine whether FIE is regulated at the translational or posttranslational levels. The objectives of our research program have been accomplished and the results obtained exceeded our expectation. Our results reveal that fie and mea mutations cause parent-of-origin effects on seed development by distinct mechanisms (Publication 1). Moreover our data show that FIE has additional functions besides controlling the development of the female gametophyte. Using transgenic lines in which FIE was not expressed or the protein level was reduced during different developmental stages enabled us for the first time to explore FIE function during sporophyte development (Publication 2 and 3). Our results are consistent with the hypothesis that FIE, a single copy gene in the Arabidopsis genome, represses multiple developmental pathways (i.e., endosperm, embryogenesis, shot formation and flowering). Furthermore, we identified FIE target genes, including key transcription factors known to promote flowering (AG and LFY) as well as shoot and leaf formation (KNAT1) (Publication 2 and 3), thus demonstrating that in plants, as in mammals and insects, PcG proteins control expression of homeobox genes. Using the Yeast two hybrid system and pull-down assays we demonstrated that FIE protein interact with MEA via the N-terminal region (Publication 1). Moreover, CURLY LEAF protein, an additional member of the SET domain family interacts with FIE as well. The overlapping expression patterns of FIE, with ether MEA or CLF and their common mutant phenotypes, demonstrate the versatility of FIE function. FIE association with different SET domain polycomb proteins, results in differential regulation of gene expression throughout the plant life cycle (Publication 3). In vitro interaction assays we have recently performed demonstrated that FIE interacts with the cell cycle regulatory component Retinobalsoma protein (pRb) (Publication 4). These results illuminate the potential mechanism by which FIE may restrain embryo sac central cell division, at least partly, through interaction with, and suppression of pRb-regulated genes. The results of this program generated new information about the initiation of reproductive development and expanded our understanding of how PcG proteins regulate developmental programs along the plant life cycle. The tools and information obtained in this program will lead to novel strategies which will allow to mange crop plants and to increase crop production.
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Ohad, Nir, and Robert Fischer. Control of Fertilization-Independent Development by the FIE1 Gene. United States Department of Agriculture, August 2000. http://dx.doi.org/10.32747/2000.7575290.bard.
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A fundamental problem in biology is to understand how fertilization initiates reproductive development. During plant reproduction, one sperm cell fuses with the egg to form an embryo, whereas a second sperm cell fuses with the adjacent central cell nucleus to form the endosperm tissue that supports embryo and/or seedling development. To understand the mechanisms that initiate reproduction, we have isolated mutants of Arabidopsis that allow for replication of the central cell and subsequent endosperm development without fertilization. In this project we have cloned the MEA gene and showed that it encode a SET- domain polycomb protein. Such proteins are known to form chromatin-protein complexes that repress homeotic gene transcription and influence cell proliferation from Drosophylla to mammals. We propose a model whereby MEA and an additional polycomb protein we have cloned, FIE , function to suppress a critical aspect of early plant reproduction and endosperm development, until fertilization occurs. Using a molecular approach we were able to determine that FIE and MEA interact physically, suggesting that these proteins have been conserved also during the evolution of flowering plants. The analysis of MEA expression pattern revealed that it is an imprinted gene that displays parent-of- origin-dependent monoallelic expression specifically in the endosperm tissue. Silencing of the paternal MEA allele in the endosperm and the phenotype of mutant mea seeds support the parental conflict theory for the evolution of imprinting in plants and mammals. These results contribute new information on the initiation of endosperm development and provide a unique entry point to study asexual reproduction and apomixis which is expected to improve crop production.
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Ori, Naomi, and Mark Estelle. Specific mediators of auxin activity during tomato leaf and fruit development. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7597921.bard.
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The plant hormone auxin is involved in numerous developmental processes, including leaf and fruit development. The tomato (Solanumlycopersicum) gene ENTIRE (E) encodes an auxin-response inhibitor from the Aux/IAA family. While most loss-offunction mutations in Aux/IAA genes are similar to the wild type due to genetic redundancy, entire (e) mutants show specific effects on leaf and fruit development. e mutants have simple leaves, in contrast to the compound leaves of wild type tomatoes. In addition, e plants produce parthenocarpic fruits, in which fruit set occurs independently of fertilization. The aim of this research program was to utilize the e mutation to identify and characterize genes that mediate the specific effect of auxin in leaf and fruit development. The specific objectives of the project were to: 1. Characterize and map modifiers of the e leaf phenotype. 2. Characterize and map suppressors of the e fruit phenotype. 3. Dissect the developmental specificity of the E gene. 4. Examine the effect of fruit-overexpression of identified genes on fruit set and seed production. To identify mediators of auxin in leaf development, we mainly focused on one mutant, crawling elephant (crel, previously called t282), which showed substantial suppression of the e phenotype and other auxin-relatedphenotypes. We have identified the CREL gene as a homolog of the Arabidopsis VRN5 gene, involved in recruiting polycomb silencing complexes to specific targets. We showed that CREL affects auxin sensitivity in tomato. Suppressors of the e fruit phenotype have been further characterized and selected for more profound effects. Expression profiling by RNAseq was used to analyze the effect of e as well as crel on gene expression in leaves and fruits. This analysis has identified putative E and CREL targets. We have initiated studies to assess the role of some of these targets in flower and fruit development. The research has identified potential mediators of auxin response in leaf, flower and fruit development.