Literatura científica selecionada sobre o tema "Xist RNA"
Crie uma referência precisa em APA, MLA, Chicago, Harvard, e outros estilos
Consulte a lista de atuais artigos, livros, teses, anais de congressos e outras fontes científicas relevantes para o tema "Xist RNA".
Ao lado de cada fonte na lista de referências, há um botão "Adicionar à bibliografia". Clique e geraremos automaticamente a citação bibliográfica do trabalho escolhido no estilo de citação de que você precisa: APA, MLA, Harvard, Chicago, Vancouver, etc.
Você também pode baixar o texto completo da publicação científica em formato .pdf e ler o resumo do trabalho online se estiver presente nos metadados.
Artigos de revistas sobre o assunto "Xist RNA"
1
Clemson, C. M., J. A. McNeil, H. F. Willard e J. B. Lawrence. "XIST RNA paints the inactive X chromosome at interphase: evidence for a novel RNA involved in nuclear/chromosome structure." Journal of Cell Biology 132, n.º 3 (1 de fevereiro de 1996): 259–75. http://dx.doi.org/10.1083/jcb.132.3.259.
Texto completo da fonteResumo:
The XIST gene is implicated in X chromosome inactivation, yet the RNA contains no apparent open reading frame. An accumulation of XIST RNA is observed near its site of transcription, the inactive X chromosome (Xi). A series of molecular cytogenetic studies comparing properties of XIST RNA to other protein coding RNAs, support a critical distinction for XIST RNA; XIST does not concentrate at Xi simply because it is transcribed and processed there. Most notably, morphometric and 3-D analysis reveals that XIST RNA and Xi are coincident in 2- and 3-D space; hence, the XIST RNA essentially paints Xi. Several results indicate that the XIST RNA accumulation has two components, a minor one associated with transcription and processing, and a spliced major component, which stably associates with Xi. Upon transcriptional inhibition the major spliced component remains in the nucleus and often encircles the extra-prominent heterochromatic Barr body. The continually transcribed XIST gene and its polyadenylated RNA consistently localize to a nuclear region devoid of splicing factor/poly A RNA rich domains. XIST RNA remains with the nuclear matrix fraction after removal of chromosomal DNA. XIST RNA is released from its association with Xi during mitosis, but shows a unique highly particulate distribution. Collective results indicate that XIST RNA may be an architectural element of the interphase chromosome territory, possibly a component of nonchromatin nuclear structure that specifically associates with Xi. XIST RNA is a novel nuclear RNA which potentially provides a specific precedent for RNA involvement in nuclear structure and cis-limited gene regulation via higher-order chromatin packaging.
2
Creamer, K. M., e J. B. Lawrence. "XIST RNA: a window into the broader role of RNA in nuclear chromosome architecture". Philosophical Transactions of the Royal Society B: Biological Sciences 372, n.º 1733 (25 de setembro de 2017): 20160360. http://dx.doi.org/10.1098/rstb.2016.0360.
Texto completo da fonteResumo:
XIST RNA triggers the transformation of an active X chromosome into a condensed, inactive Barr body and therefore provides a unique window into transitions of higher-order chromosome architecture. Despite recent progress, how XIST RNA localizes and interacts with the X chromosome remains poorly understood. Genetic engineering of XIST into a trisomic autosome demonstrates remarkable capacity of XIST RNA to localize and comprehensively silence that autosome. Thus, XIST does not require X chromosome-specific sequences but operates on mechanisms available genome-wide. Prior results suggested XIST localization is controlled by attachment to the insoluble nuclear scaffold. Our recent work affirms that scaffold attachment factor A (SAF-A) is involved in anchoring XIST , but argues against the view that SAF-A provides a unimolecular bridge between RNA and the chromosome. Rather, we suggest that a complex meshwork of architectural proteins interact with XIST RNA. Parallel work studying the territory of actively transcribed chromosomes suggests that repeat-rich RNA ‘coats’ euchromatin and may impact chromosome architecture in a manner opposite of XIST . A model is discussed whereby RNA may not just recruit histone modifications, but more directly impact higher-order chromatin condensation via interaction with architectural proteins of the nucleus. This article is part of the themed issue ‘X-chromosome inactivation: a tribute to Mary Lyon’.
3
Rodermund, Lisa, Heather Coker, Roel Oldenkamp, Guifeng Wei, Joseph Bowness, Bramman Rajkumar, Tatyana Nesterova, David Miguel Susano Pinto, Lothar Schermelleh e Neil Brockdorff. "Time-resolved structured illumination microscopy reveals key principles of Xist RNA spreading". Science 372, n.º 6547 (10 de junho de 2021): eabe7500. http://dx.doi.org/10.1126/science.abe7500.
Texto completo da fonteResumo:
X-inactive specific transcript (Xist) RNA directs the process of X chromosome inactivation in mammals by spreading in cis along the chromosome from which it is transcribed and recruiting chromatin modifiers to silence gene transcription. To elucidate mechanisms of Xist RNA cis-confinement, we established a sequential dual-color labeling, super-resolution imaging approach to trace individual Xist RNA molecules over time, which enabled us to define fundamental parameters of spreading. We demonstrate a feedback mechanism linking Xist RNA synthesis and degradation and an unexpected physical coupling between preceding and newly synthesized Xist RNA molecules. Additionally, we find that the protein SPEN, a key factor for Xist-mediated gene silencing, has a distinct function in Xist RNA localization, stability, and coupling behaviors. Our results provide insights toward understanding the distinct dynamic properties of Xist RNA.
4
Clemson, Christine Moulton, Jennifer C. Chow, Carolyn J. Brown e Jeanne Bentley Lawrence. "Stabilization and Localization of Xist RNA are Controlled by Separate Mechanisms and are Not Sufficient for X Inactivation". Journal of Cell Biology 142, n.º 1 (13 de julho de 1998): 13–23. http://dx.doi.org/10.1083/jcb.142.1.13.
Texto completo da fonteResumo:
These studies address whether XIST RNA is properly localized to the X chromosome in somatic cells where human XIST expression is reactivated, but fails to result in X inactivation (Tinker, A.V., and C.J. Brown. 1998. Nucl. Acids Res. 26:2935–2940). Despite a nuclear RNA accumulation of normal abundance and stability, XIST RNA does not localize in reactivants or in naturally inactive human X chromosomes in mouse/ human hybrid cells. The XIST transcripts are fully stabilized despite their inability to localize, and hence XIST RNA localization can be uncoupled from stabilization, indicating that these are separate steps controlled by distinct mechanisms. Mouse Xist RNA tightly localized to an active X chromosome, demonstrating for the first time that the active X chromosome in somatic cells is competent to associate with Xist RNA. These results imply that species-specific factors, present even in mature, somatic cells that do not normally express Xist, are necessary for localization. When Xist RNA is properly localized to an active mouse X chromosome, X inactivation does not result. Therefore, there is not a strict correlation between Xist localization and chromatin inactivation. Moreover, expression, stabilization, and localization of Xist RNA are not sufficient for X inactivation. We hypothesize that chromosomal association of XIST RNA may initiate subsequent developmental events required to enact transcriptional silencing.
5
Coker, Heather, Guifeng Wei, Benoit Moindrot, Shabaz Mohammed, Tatyana Nesterova e Neil Brockdorff. "The role of the Xist 5’ m6A region and RBM15 in X chromosome inactivation". Wellcome Open Research 5 (17 de fevereiro de 2020): 31. http://dx.doi.org/10.12688/wellcomeopenres.15711.1.
Texto completo da fonteResumo:
Background: X chromosome inactivation in mammals is regulated by the non-coding (nc) RNA, Xist, which represses the chromosome from which it is transcribed. High levels of the N6-methyladenosine (m6A) RNA modification occur within Xist exon I, close to the 5’ end of the transcript, and also further 3’, in Xist exon VII. The m6A modification is catalysed by the METTL3/14 complex that is directed to specific targets, including Xist, by the RNA binding protein RBM15/15B. m6A modification of Xist RNA has been reported to be important for Xist–mediated gene silencing. Methods: We use CRISPR/Cas9 mediated mutagenesis to delete sequences around the 5’ m6A region in interspecific XX mouse embryonic stem cells (mESCs). Following induction of Xist RNA expression, we assay chromosome silencing using allelic RNA-seq and Xist m6A distribution using m6A-seq. Additionally, we use Xist RNA FISH to analyse the effect of deleting the 5’ m6A region on the function of the endogenous Xist promoter. We purify epitope tagged RBM15 from mESCs, and then apply MS/MS analysis to define the RBM15 interactome. Results: We show that a deletion encompassing the entire Xist 5’ m6A region results in a modest reduction in Xist-mediated silencing, and that the 5’ m6A region overlaps essential DNA elements required for activation of the endogenous Xist promoter. Deletion of the Xist A-repeat, to which RBM15 binds, entirely abolishes deposition of m6A in the Xist 5’ m6A region without affecting the modification in exon VII. We show that in mESCs, RBM15 interacts with the m6A complex, the SETD1B histone modifying complex, and several proteins linked to RNA metabolism. Conclusions: Our findings support that RBM15 binding to the Xist A-repeat recruits the m6A complex to the 5’ Xist m6A region and that this region plays a role in Xist-mediated chromosome silencing.
6
Jonkers, Iris, Kim Monkhorst, Eveline Rentmeester, J. Anton Grootegoed, Frank Grosveld e Joost Gribnau. "Xist RNA Is Confined to the Nuclear Territory of the Silenced X Chromosome throughout the Cell Cycle". Molecular and Cellular Biology 28, n.º 18 (14 de julho de 2008): 5583–94. http://dx.doi.org/10.1128/mcb.02269-07.
Texto completo da fonteResumo:
ABSTRACT In mammalian female cells, one X chromosome is inactivated to prevent a dose difference in the expression of X-encoded proteins between males and females. Xist RNA, required for X chromosome inactivation, is transcribed from the future inactivated X chromosome (Xi), where it spreads in cis, to initiate silencing. We have analyzed Xist RNA transcription and localization throughout the cell cycle. It was found that Xist transcription is constant and that the mature RNA remains attached to the Xi throughout mitosis. Diploid and tetraploid cell lines with an MS2-tagged Xist gene were used to investigate spreading of Xist. Most XXXXMS2 tetraploid mouse embryonic stem (ES) cells inactivate the XMS2 chromosome and one other X chromosome. Analysis of cells with two Xi's indicates that Xist RNA is retained by the Xi of its origin and does not spread in trans. Also, in XXMS2 diploid mouse ES cells with an autosomal Xist transgene, there is no trans exchange of Xist RNA from the Xi to the autosome. We propose that Xist RNA does not dissociate from the Xi of its origin, which precludes a model of diffusion-mediated trans spreading of Xist RNA.
7
Hall, Lisa L., Meg Byron, Gayle Pageau e Jeanne B. Lawrence. "AURKB-mediated effects on chromatin regulate binding versus release of XIST RNA to the inactive chromosome". Journal of Cell Biology 186, n.º 4 (24 de agosto de 2009): 491–507. http://dx.doi.org/10.1083/jcb.200811143.
Texto completo da fonteResumo:
How XIST RNA strictly localizes across the inactive X chromosome is unknown; however, prophase release of human XIST RNA provides a clue. Tests of inhibitors that mimic mitotic chromatin modifications implicated an indirect role of PP1 (protein phosphatase 1), potentially via its interphase repression of Aurora B kinase (AURKB), which phosphorylates H3 and chromosomal proteins at prophase. RNA interference to AURKB causes mitotic retention of XIST RNA, unlike other mitotic or broad kinase inhibitors. Thus, AURKB plays an unexpected role in regulating RNA binding to heterochromatin, independent of mechanics of mitosis. H3 phosphorylation (H3ph) was shown to precede XIST RNA release, whereas results exclude H1ph involvement. Of numerous Xi chromatin (chromosomal protein) hallmarks, ubiquitination closely follows XIST RNA retention or release. Surprisingly, H3S10ph staining (but not H3S28ph) is excluded from Xi and is potentially linked to ubiquitination. Results suggest a model of multiple distinct anchor points for XIST RNA. This study advances understanding of RNA chromosome binding and the roles of AURKB and demonstrates a novel approach to manipulate and study XIST RNA.
8
Shestakova, E. A., e T. A. Bogush. "BRCA1 participates in the expression of noncoding XIST RNA". Russian Journal of Biotherapy 18, n.º 1 (19 de abril de 2019): 67–74. http://dx.doi.org/10.17650/1726-9784-2019-18-1-67-74.
Texto completo da fonteResumo:
Introduction . Noncoding RNA of XIST gene (X inactivation-specific transcript) initiates inactivation of one of X chromosomes in cells of female organism. Further stages of this process include chromatin epigenetic modifications leading to the inhibition of the most genes on X chromosome. Recently the data were obtained that tumor suppressor BRCA1 is associated with inactive X chromosome (Xi) participating in XIST RNA localization on Xi and influencing XIST RNA expression.Objective: to reveal the role of BRCA1 in XIST RNA expression.Materials and methods . The objects of the study were mutant breast cancer cell lines (BRCA1–/–): HCC1395, HCC1937, SUM149PT, and, as controls – cell lines containing wild type of BRCA1 gene (BRCA1+/+): IMR90 и 293T. Method of reverse transcription coupled with polymerase chain reaction (RT-PCR) was used for the analysis of XIST RNA expression.Results . In the clone of doxycycline-inducible HCC1937 breast cancer cell line XIST RNA expression was observed upon BRCA1 induction. In HCC1395, HCC1937 and SUM149PT breast cancer cell lines containing mutant BRCA1 gene (BRCA1–/–) and nonfunctional BRCA1 protein the absence of XIST RNA expression was observed using RT-PCR. This observation indicates the indispensable role of functional BRCA1 protein in XIST RNA expression.Conclusion . Altogether, the data obtained in this study confirm the role of BRCA1 in the expression of noncoding inhibiting XIST RNA and suggest the involvement of BRCA1 in the inhibition of gene expression on Xi.
9
Coker, Heather, Benoit Moindrot, Greta Pintacuda e Neil Brockdorff. "Illuminating Xist". Biochemist 37, n.º 2 (1 de abril de 2015): 24–27. http://dx.doi.org/10.1042/bio03702024.
Texto completo da fonteResumo:
The Central Dogma proposed that RNA, encoded by DNA in the genome, acts as the template used by cells for protein production. The simplicity of RNA as a discrete mediator of information has subsequently been challenged by the discovery of non-protein-coding RNAs. Understanding of this intricate new field has been fuelled by the development of new research techniques. In this article, we consider how recent advances in microscopy have added to our current understanding of the non-coding RNA Xist (X-inactive specific transcript).
10
Jiang, Di. "Visualizing Xist RNA dynamics". Science 372, n.º 6547 (10 de junho de 2021): 1162.11–1164. http://dx.doi.org/10.1126/science.372.6547.1162-k.
Texto completo da fonteTeses / dissertações sobre o assunto "Xist RNA"
1
Kelsey, Angela. "Mechanisms for XIST RNA cis-localisation". Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/44992.
Texto completo da fonteResumo:
X inactivation is the process of silencing one of the two X chromosomes in mammalian female cells in order to equalise the dosage of X-linked genes with males. The process is initiated by the long noncoding RNA XIST, which is transcribed from the future inactive X and localises to it in cis. How XIST RNA is able to localise to the X chromosome is not well defined. The aim of the current study was to deduce mechanisms of XIST RNA localisation. This was addressed in various ways, including 1) testing the ability of an XIST transgene integrated into a variety of autosomes to localise to those autosomes, as opposed to the X chromosome; 2) assessing the ability of XIST transgenes with different regions deleted to localise, in order to identify sequences required for localisation; and 3) knocking down various proteins implicated in X inactivation in order to assess any effect on the ability of XIST to localise. We find that the XIST transgene is able to localise to a wide variety of different autosomes and furthermore, is able to direct the enrichment of the histone variant macroH2A on an autosome and the deposition of a repressive histone modification, H3K27me3, onto an autosome. We also find that a region of XIST encompassing repeats B and C, and sequences downstream of exon 1 are involved in localising XIST RNA, and that they do so in a redundant fashion. Lastly, we show that the knockdown of five proteins - YY1, hnRNP-U, SPOP, CUL3 and ASH2L - prevent the formation of an intact XIST focus. The results presented here add to the limited knowledge of how XIST RNA is able to localise, an essential step in the process of X chromosome inactivation.
2
Minks, Jakub. "Role of XIST RNA and its interacting protein partners in gene silencing". Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/42837.
Texto completo da fonteResumo:
X-chromosome inactivation ensures equal expression of mammalian male and female X-linked genes by transcriptionally silencing one X chromosome in each female cell. The pivotal molecule responsible for the silencing is a long non-coding RNA XIST; however, an all-encompassing model explaining how XIST induces silencing of the whole X chromosome is yet to emerge. This thesis aims to broaden our understanding of XIST action in humans by leveraging an inducible XIST transgene capable of silencing downstream reporters to identify sequences within XIST and XIST-interacting proteins critical for gene silencing.
First, we demonstrate that the repeat A region of XIST is necessary and sufficient to induce gene silencing, at least locally, irrespective of the makeup of the surrounding chromatin, and that XIST induces silencing of a distal gene in one of the HT1080 cell lines. Second, we show that individual repeats of a consensus repeat A sequence contribute additively to silencing. Mutations within a construct consisting of two repeat A units both demonstrate that the two palindromic sequences within the repeat A units spanning ‘ATCG’ and ‘ATAC’ tetranucleotides are critical for repeat A function and add to the evidence that the first palindrome forms a hairpin, rather than engaging in pairing between repeat A units.
Third, we explore which proteins are critical for XIST-induced silencing. We show that histone deacetylation, an early mark of an X-chromosome inactivation, is likely a consequence, and not the cause of XIST-induced silencing. We next demonstrate that in the transgenic HT1080 system, gene silencing is not accompanied by recruitment of the H3K27me3 repressive histone mark and XIST induces silencing independently of its previously reported associations with the polycomb repressive complex 2 (PRC2). Finally, we performed siRNA-mediated knock-down of 31 proteins previously implicated to play a role in X-chromosome inactivation. Our results show that proteins involved in XIST RNA localization (YY1), chromatin organization (SATB2, HNRNPU), and cell cycle (ATM), as well as an E3 ubiquitin ligase (SPOP) contribute to XIST-induced gene silencing in the HT1080 system. Thus, we demonstrate that the repeat A alone induces gene silencing and identify candidate pathways critical for its function.
3
Csankovszki, Györgyi 1971. "The role of Xist RNA in the maintenance of X chromosome inactivation". Thesis, Massachusetts Institute of Technology, 2001. http://hdl.handle.net/1721.1/8209.
Texto completo da fonteResumo:
Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2001.Includes bibliographical references.
The role of Xist RNA in silencing the inactive X of female somatic cells was investigated by generating a conditional allele of the Xist gene. A system was set up in which reactivation of two X-linked genes, the endogenous Hprt gene and an X-linked GFP transgene, can be quantitatively assessed. Mouse embryonic fibroblasts derived from mice carrying the conditional Xist mutation were cultured and infected with an adenovirus vector carrying the gene for Cre recombinase. After Cre mediated deletion of Xist, the inactive X remained transcriptionally silent, late replicating, and hypoacetylated on histone H4, confirming that X-inactivation can be maintained in the absence of Xist RNA. However, the Xist mutant inactive X was no longer enriched in histone macroH2A 1. Furthermore, the reactivation rate of GFP and Hprt increased, indicating Xist RNA does contribute to gene repression on the inactive X. DNA methylation, histone hypoacetylation and Xist RNA were found to act synergistically in X chromosome silencing. To investigate whether Xist RNA can also silence the active X chromosome of male somatic cells, Xist expression on the active X was induced by demethylation. Demethylation was achieved by Cre mediated deletion of a conditional mutant allele of DNA methyltransferase-l (Dnmtl) in male fibroblasts. In these cells, Xist RNA coated the active X chromosome, in a pattern indistinguishable from coating of the inactive X of female cells. Although many Xist expressing chromosomes also transcribed X-linked genes Pgk-i and Hprt, in a small percent of cells Xist expression led to X chromosome inactivation. The proportion of chromosome expressing X-linked genes declined, and occasionally the X became late replicating, indicating that X-inactivation can be initiated in male somatic cells.
by Györgyi Csankovszki.
Ph.D.
4
Tang, Yuen-Man Amy. "The influence of genome environment on Xist RNA-Mediated gene silencing in autosomes". Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.435176.
Texto completo da fonte
5
Furlan, Giulia. "Investigating the contribution of the non-coding gene Ftx to X-chromosome inactivation in mammals". Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCC191/document.
Texto completo da fonteResumo:
L’inactivation du chromosome X (XCI) est un mécanisme qui permet l’extinction transcriptionelle d’un des deux chromosomes X chez la femelle. XCI est régulé par une région spécifique nommée centre de l’inactivation du chromosome (Xic), contenant plusieurs gènes produisant de longs ARNs non codants (lncRNAs). Parmi ces lncRNAs, le transcrit Xist est l’effecteur principal pour l’XCI. Xist peut s’accumuler en cis sur le chromosome et recruter la machinerie qui permettra l’initiation et la propagation de l’extinction transcriptionnelle à l’échelle du chromosome.Le laboratoire d’accueil a identifié un nouveau gène du Xic qui produit le lncRNA Ftx. Dans cette étude, on a pu montrer que l’inactivation du chromosome X est fortement perturbée dans les cellules Ftx-/- et s’accompagne par une forte baisse du niveau d’expression et d’accumulation de Xist. Dans ce contexte, certaines cellules parviennent à maintenir l’expression de Xist mais le profil de couverture du chromosome X par Xist est anormal, présentant un profil diffus ; ceci est associé à une extinction transcriptionnelle déficiente des gènes liés à l’X. Dans les lignées hétérozygotes Ftx+/-, l’expression et l’accumulation de Xist est aussi affectée mais dans une moindre mesure, si bien qu’il apparaît que le nombre de copies de Ftx soit important pour sa fonction. Par ailleurs, l’inactivation du chromosome X dans les cellules Ftx+/- est biaisée de telle sorte que le chromosome X portant une copie fonctionnelle de Ftx est préférentiellement inactivé, suggérant un rôle en cis de Ftx. Ces résultats montrent que Ftx est un activateur de Xist et qu’il est essentiel pour la mise en place de l’inactivationX-chromosome inactivation (XCI) is a female-specific, chromosome-wide regulatory process that, in eutherians, ensures dosage compensation for X-linked genes between sexes. XCI is controlled by a cis-acting locus on the X-chromosome, the X-inactivation center (Xic), enriched in genes producing long non-coding RNAs (lncRNAs). The Xic-linked gene Xist is the master player of XCI, and produces a lncRNA that accumulates in cis on the X-chromosome and recruits the machinery responsible for initiation and propagation of silencing.The laboratory has identified an additional Xic-linked non-coding gene, Ftx. In this study, we could find that, in female Ftx-/- lines, XCI is strongly impaired, with a significant decrease in the levels of Xist expression and in the percentage of cells showing normal Xist accumulation patterns. Importantly, a high proportion of the cells that still retain Xist expression show abnormal X-chromosome coating and a decreased ability to silence X-linked genes. These data reveal that Ftx is a positive Xist regulator and it is required for proper XCI establishment. In female Ftx+/- lines, the levels of Xist expression and the percentage of cells showing normal Xist accumulation patterns are also decreased, albeit to a lower extent compared to Ftx-/- lines, suggesting that Ftx works in a copy-dependent manner. In addition, a high proportion of Ftx+/- cells display skewed X-inactivation, with preferential inactivation of the wild-type X chromosome. This suggests that Ftx role on Xist accumulation is mostly restricted in cis. Taken together, these results demonstrate that Ftx is required for XCI establishment, where it functions as a strong Xist activator
6
Li, Yue. "Chemical biology studies on the structures and biological functions of nucleic acids". 京都大学 (Kyoto University), 2016. http://hdl.handle.net/2433/215340.
Texto completo da fonte
7
Clemson, Christine Moulton. "Structural Association of XIST RNA with Inactive Chromosomes in Somatic Cells : a Key Step in the Process that Establishes and Faithfully Maintains X-inactivation". eScholarship@UMMS, 1998. https://escholarship.umassmed.edu/gsbs_diss/8.
Texto completo da fonteResumo:
The XIST gene is implicated in X-chromosome inactivation, yet the RNA contains no apparent open reading frame. An accumulation of XIST RNA is observed near its site of transcription, the inactive X chromosome (Xi). A series of molecular cytogenetic studies comparing properties of XIST RNA to other protein coding RNAs, support a critical distinction for XIST RNA; XIST RNA does not concentrate at Xi simply because it is transcribed and processed there. Most notably, morphometric and 3-D analysis reveals that XIST RNA and Xi are coincident in 2-D and 3-D space; hence the XIST RNA essentially paints Xi. Several results indicate that the XIST RNA accumulation has two components, a minor one associated with transcription and processing, and a spliced major component, which stably associates with Xi. Upon transcriptional inhibition the major spliced component remains in the nucleus and often encircles the extra-prominent heterochromatic Barr body. The continually transcribed XIST gene and its poly-adenylated RNA consistently localize to a nuclear region devoid of splicing factor/poly A RNA rich domains. XIST RNA remains with the nuclear matrix fraction after removal of chromosomal DNA. XIST RNA is released from its association with Xi during mitosis, but shows a unique highly particulate distribution. Collective results indicate that XIST RNA may be an architectural element of the interphase chromosome territory, possibly a component of non-chromatin nuclear structure that specifically associates with Xi. XIST RNA is a novel nuclear RNA which potentially provides a specific precedent for RNA involvement in nuclear structure and cis-limited gene regulation via higher-order chromatin packaging.
8
Salvador, Marion. "Régulation épigénétique des cellules souches cancéreuses mammaires : un nouveau rôle pour l'ARN non-codant Xist". Thesis, Aix-Marseille, 2014. http://www.theses.fr/2014AIXM5078.
Texto completo da fonteResumo:
La récidive et la progression métastatique du cancer du sein ne sont toujours pas curables. Le concept des cellules souches cancéreuses (CSC) pourrait apporter une explication à ces échecs. Les CSC résisteraient aux thérapies conventionnelles (chimiothérapies, radiothérapie) et seraient responsables de la rechute et de la progression du cancer. L'élimination des CSC semble être un pré-requis indispensable pour le traitement des patientes. L'identité et le destin des cellules souches sont finement régulés par des acteurs épigénétiques. Les travaux de cette thèse se sont intéressés aux conséquences de la dérégulation de deux acteurs épigénétiques en particulier : les enzymes HDAC et le long ARN non-codant Xist. Nous avons montré que la modulation épigénétique via l'inhibition des HDAC (HDACi) permet d'éliminer les CSC en induisant leur différenciation. Nous présentons une nouvelle stratégie thérapeutique pour le cancer du sein : la thérapie différenciante. Nous avons déterminé Xist comme étant le biomarqueur prédictif de la réponse aux HDACi. Xist étant un partenaire clé de la plasticité cellulaire, les travaux de cette thèse se sont ensuite intéressés aux conséquences de la dérégulation de Xist dans l'initiation tumorale. Nous avons observé que l'inhibition de Xist favorise la division des cellules souches mammaires normales. Nous proposons un nouveau modèle de l'initiation tumorale où la dérégulation épigénétique est une modification précoce sans conséquence sur l'homéostasie tissulaire mais pourrait être la première étape de la transformation cancéreuseThese last decades have allowed deciphering the biology of breast cancer and improving the therapeutic management. However, recurrence and metastatic progression of the disease are still not curable. The concept of cancer stem cells (CSC) could provide an explanation for these failures. CSC would resist conventional therapies (chemotherapy, radiotherapy) and would be responsible for both relapse and progression of cancer. The elimination of CSC seems to be an essential prerequisite for the treatment of patients. The identity and fate of stem cells are tightly regulated by epigenetic mechanisms. The work of this thesis investigated the consequences of deregulation of two epigenetic players: HDAC enzymes and long non-coding RNA Xist. We have shown that epigenetic modulation via HDAC inhibitor (HDACi) eliminates the CSC by inducing their differentiation. We present a new therapeutic strategy for breast cancer: differentiation therapy. We determined Xist as the predictive biomarker of response to HDACi. Xist is a key partner of cell plasticity, the work of this thesis therefore interested in the consequences of Xist deregulation in tumor initiation. We observed that Xist inhibition promotes division of normal breast stem cells. We propose a new model of tumor initiation: epigenetic deregulation is an early change without consequence on tissue homeostasis but could be the first step of the cancerous transformation
9
Smeets, Daniel [Verfasser], e Heinrich [Akademischer Betreuer] Leonhardt. "Analysis of the Barr body with super-resolution microscopy : implications for a structural role of Xist RNA in mammalian X chromosome inactivation / Daniel Smeets. Betreuer: Heinrich Leonhardt". München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2013. http://d-nb.info/1045561339/34.
Texto completo da fonte
10
Kolpa, Heather J. "XIST and CoT-1 Repeat RNAs are Integral Components of a Complex Nuclear Scaffold Required to Maintain SAF-A and Modify Chromosome Architecture: A Dissertation". eScholarship@UMMS, 2004. http://escholarship.umassmed.edu/gsbs_diss/825.
Texto completo da fonteResumo:
XIST RNA established the precedent for a noncoding RNA that stably associates with and regulates chromatin, however it remains poorly understood how such RNAs structurally associate with the interphase chromosome territory. I demonstrate that transgenic XIST RNA localizes in cis to an autosome as it does to the inactive X chromosome, hence the RNA recognizes a structure common to all chromosomes. I reassess the prevalent thinking in the field that a single protein, Scaffold Attachment Factor-A (SAF-A/hnRNP U), provides a single molecule bridge required to directly tether the RNA to DNA. In an extensive series of experiments in multiple cell types, I examine the effects of SAF-A depletion or different SAF-A mutations on XIST RNA localization, and I force XIST RNA retention at mitosis to examine the effect on SAF-A. I find that SAF-A is not required to localize XIST RNA but is one of multiple proteins involved, some of which frequently become lost or compromised in cancer. I additionally examine SAF-A’s potential role localizing repeat-rich CoT-1 RNA, a class of abundant RNAs that we show tightly and stably localize to euchromatic interphase chromosome territories, but release upon disruption of the nuclear scaffold. Overall, findings suggest that instead of “tethering” chromosomal RNAs to the scaffold, SAF-A is one component of a multi-component matrix/scaffold supporting interphase nuclear architecture. Results indicate that Cot-1 and XIST RNAs form integral components of this scaffold and are required to maintain the chromosomal association of SAF-A, substantially advancing understanding of how chromatin-associated RNAs contribute to nuclear structure.
Capítulos de livros sobre o assunto "Xist RNA"
1
Masui, Osamu, Edith Heard e Haruhiko Koseki. "Live Imaging of Xist RNA". In Methods in Molecular Biology, 67–72. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8766-5_6.
Texto completo da fonte
2
Waśko, Urszula, Zeming Zheng e Sanchita Bhatnagar. "Visualization of Xist Long Noncoding RNA with a Fluorescent CRISPR/Cas9 System". In Epitranscriptomics, 41–50. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8808-2_3.
Texto completo da fonte
3
Yamada, Norishige, e Yuya Ogawa. "Mechanisms of Long Noncoding Xist RNA-Mediated Chromosome-Wide Gene Silencing in X-Chromosome Inactivation". In Long Noncoding RNAs, 151–71. Tokyo: Springer Japan, 2015. http://dx.doi.org/10.1007/978-4-431-55576-6_9.
Texto completo da fonte
4
Lucchesi, John C. "Regulation of domains and whole chromosomes". In Epigenetics, Nuclear Organization & Gene Function, 104–22. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198831204.003.0009.
Texto completo da fonteResumo:
Clusters of genes that encode similar products, such as the β-globin, the ribosomal RNA (rRNA) and the histone genes, are regulated in a coordinated fashion. An extreme case of coordinate regulation—dosage compensation—involves the genes present on the sex chromosomes. In Drosophila males, a complex (MSL) associates with the X chromosome where it enhances the activity of most X-linked genes. In Caenorhabditis, a complex (DCC) decreases the level of transcription of both X chromosomes in the XX hermaphrodite. In mammals, dosage compensation is achieved by the inactivation, early during development, of most X-linked genes on one of the two X chromosomes in females. In the mammalian embryo, X inactivation of either X chromosome is random and clonally inherited. The mechanism involves the synthesis of an RNA (Tsix) that protects one of the two Xs from inactivation, and of another RNA (Xist) that coats the other X chromosome and recruits histone- and DNA-modifying enzymes.