Academic literature on the topic 'Convergent transcription'
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Journal articles on the topic "Convergent transcription"
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Hobson, David J., Wu Wei, Lars M. Steinmetz, and Jesper Q. Svejstrup. "RNA Polymerase II Collision Interrupts Convergent Transcription." Molecular Cell 48, no. 3 (November 2012): 365–74. http://dx.doi.org/10.1016/j.molcel.2012.08.027.
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Gullerova, Monika, and Nick J. Proudfoot. "Convergent transcription induces transcriptional gene silencing in fission yeast and mammalian cells." Nature Structural & Molecular Biology 19, no. 11 (September 30, 2012): 1193–201. http://dx.doi.org/10.1038/nsmb.2392.
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Lin, Yunfu, Mei Leng, Ma Wan, and John H. Wilson. "Convergent Transcription through a Long CAG Tract Destabilizes Repeats and Induces Apoptosis." Molecular and Cellular Biology 30, no. 18 (July 20, 2010): 4435–51. http://dx.doi.org/10.1128/mcb.00332-10.
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ABSTRACT Short repetitive sequences are common in the human genome, and many fall within transcription units. We have previously shown that transcription through CAG repeat tracts destabilizes them in a way that depends on transcription-coupled nucleotide excision repair and mismatch repair. Recent observations that antisense transcription accompanies sense transcription in many human genes led us to test the effects of antisense transcription on triplet repeat instability in human cells. Here, we report that simultaneous sense and antisense transcription (convergent transcription) initiated from two inducible promoters flanking a CAG95 tract in a nonessential gene enhances repeat instability synergistically, arrests the cell cycle, and causes massive cell death via apoptosis. Using chemical inhibitors and small interfering RNA (siRNA) knockdowns, we identified the ATR (ataxia-telangiectasia mutated [ATM] and Rad3 related) signaling pathway as a key mediator of this cellular response. RNA polymerase II, replication protein A (RPA), and components of the ATR signaling pathway accumulate at convergently transcribed repeat tracts, accompanied by phosphorylation of ATR, CHK1, and p53. Cell death depends on simultaneous sense and antisense transcription and is proportional to their relative levels, it requires the presence of the repeat tract, and it occurs in both proliferating and nonproliferating cells. Convergent transcription through a CAG repeat represents a novel mechanism for triggering a cellular stress response, one that is initiated by events at a single locus in the genome and resembles the response to DNA damage.
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Inagaki, Soichi, Mayumi Takahashi, Kazuya Takashima, Satoyo Oya, and Tetsuji Kakutani. "Chromatin-based mechanisms to coordinate convergent overlapping transcription." Nature Plants 7, no. 3 (March 2021): 295–302. http://dx.doi.org/10.1038/s41477-021-00868-3.
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Dang, Yunkun, Liande Li, Wei Guo, Zhihong Xue, and Yi Liu. "Convergent Transcription Induces Dynamic DNA Methylation at disiRNA Loci." PLoS Genetics 9, no. 9 (September 5, 2013): e1003761. http://dx.doi.org/10.1371/journal.pgen.1003761.
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Lin, William Y., Yunfu Lin, and John H. Wilson. "Convergent transcription through microsatellite repeat tracts induces cell death." Molecular Biology Reports 41, no. 9 (July 11, 2014): 5627–34. http://dx.doi.org/10.1007/s11033-014-3432-y.
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Marinov, Georgi K., Alexandro E. Trevino, Tingting Xiang, Anshul Kundaje, Arthur R. Grossman, and William J. Greenleaf. "Transcription-dependent domain-scale three-dimensional genome organization in the dinoflagellate Breviolum minutum." Nature Genetics 53, no. 5 (April 29, 2021): 613–17. http://dx.doi.org/10.1038/s41588-021-00848-5.
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AbstractDinoflagellate chromosomes represent a unique evolutionary experiment, as they exist in a permanently condensed, liquid crystalline state; are not packaged by histones; and contain genes organized into tandem gene arrays, with minimal transcriptional regulation. We analyze the three-dimensional genome of Breviolum minutum, and find large topological domains (dinoflagellate topologically associating domains, which we term ‘dinoTADs’) without chromatin loops, which are demarcated by convergent gene array boundaries. Transcriptional inhibition disrupts dinoTADs, implicating transcription-induced supercoiling as the primary topological force in dinoflagellates.
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Eszterhas, Susan K., Eric E. Bouhassira, David I. K. Martin, and Steven Fiering. "Transcriptional Interference by Independently Regulated Genes Occurs in Any Relative Arrangement of the Genes and Is Influenced by Chromosomal Integration Position." Molecular and Cellular Biology 22, no. 2 (January 15, 2002): 469–79. http://dx.doi.org/10.1128/mcb.22.2.469-479.2002.
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ABSTRACT Transcriptional interference is the influence, generally suppressive, of one active transcriptional unit on another unit linked in cis. Its wide occurrence in experimental systems suggests that it may also influence transcription in many loci, but little is known about its precise nature or underlying mechanisms. Here we report a study of the interaction of two nearly identical transcription units juxtaposed in various arrangements. Each reporter gene in the constructs has its own promoter and enhancer and a strong polyadenylation signal. We used recombinase-mediated cassette exchange (RMCE) to insert the constructs into previously tagged genomic sites in cultured cells. This strategy also allows the constructs to be assessed in both orientations with respect to flanking chromatin. In each of the possible arrangements (tandem, divergent, and convergent), the presence of two genes strongly suppresses expression of both genes compared to that of an identical single gene at the same integration site. The suppression is most severe with the convergent arrangement and least severe in total with the divergent arrangement, while the tandem arrangement is most strongly influenced by the integration site and the genes’ orientation within the site. These results suggest that transcriptional interference could underlie some position effects and contribute to the regulation of genes in complex loci.
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Calero-Nieto, Fernando J., Andrew G. Bert, and Peter N. Cockerill. "Transcription-dependent silencing of inducible convergent transgenes in transgenic mice." Epigenetics & Chromatin 3, no. 1 (2010): 3. http://dx.doi.org/10.1186/1756-8935-3-3.
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Chatterjee, A., C. M. Johnson, C. C. Shu, Y. N. Kaznessis, D. Ramkrishna, G. M. Dunny, and W. S. Hu. "Convergent transcription confers a bistable switch in Enterococcus faecalis conjugation." Proceedings of the National Academy of Sciences 108, no. 23 (May 23, 2011): 9721–26. http://dx.doi.org/10.1073/pnas.1101569108.
Full textDissertations / Theses on the topic "Convergent transcription"
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Billingsley, Daniel Jeffrey. "Convergent transcription and nested gene models studied by AFM." Thesis, University of Leeds, 2012. http://etheses.whiterose.ac.uk/3149/.
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Genomic DNA is organised in complex spatial arrangements, and a given stretch of DNA may encode more than one gene. In some cases one gene may be entirely contained within a region of the DNA already occupied by another larger gene. The presence of these nested genes, often situated in introns and in the opposite orientation, poses important implications with regards to gene expression, function and regulation. A consequence of the nested gene arrangement is convergent transcription, occurring when two promoters on opposite DNA strands are active. Elucidating the mechanics of multiple interacting proteins on single DNA templates requires single molecule methods such as atomic force microscopy (AFM). AFM can accurately determine the relative positions of enzymes, such as RNA polymerase (RNAP), on individual DNA templates. The central aim of this thesis is to use AFM to study the outcomes of convergent transcription, using linear DNA templates that function as models for nested genes. Fundamental aspects of imaging DNA on mica with AFM were investigated, with a view to optimising sample preparation. The main processes involved with preparing DNA samples, ready for scanning, were examined in turn. Effective binding was achieved by introducing divalent cations into a deposition buffer. Mica ion exchanged with Ni(II) usually gave rise to kinetically-trapped DNA molecules, however short linear fragments (< 800bp) were seen to deviate from the expected behaviour, indicating that ion-exchanged mica is heterogeneous, and contains patches or domains. These findings can be used to more readily control binding of DNA to substrates. The outcomes of varying the relative humidity while imaging biomolecular systems are largely unexplored to date. Various DNA samples were imaged in conditions of varying humidity. In particular when supercoiled plasmids are scanned at very high relative humidity (> 90% RH), localised DNA backbone motions or conformational changes were observed. Humidity controlled AFM will be a useful technique for probing DNA topology without some of the drawbacks of imaging under bulk solution. Initial studies of transcription utilised templates containing two promoter sites and E. Coli RNAP. Two promoter arrangements were studied: a convergent template containing the promoter sites on opposite strands directed towards each other, and a tandem template containing the promoters in the same direction, on the same stand. It was shown that collisions between RNAPs led to similar outcomes in both cases: RNAPs are unable to pass each other and remain stalled against each other. In the convergent case, it was observed that after collision one RNAP could cause another to backtrack along the template. By end-labelling double-stranded (ds) DNA templates with a single-stranded DNA loop, the polarity of the molecules can be established in the AFM. It allowed better discrimination between outcomes of collision events on single DNA molecules and importantly, it enabled a quantitative comparison of the relative frequencies of the outcomes. The most common outcome is a collision between an actively transcribing elongation complex (EC) and a “sitting duck” (SD), which is a stalled RNAP or open promoter complex (OPC). In collisions initiated from OPCs, the most likely outcome, a collision between an EC and an SD occurs ~74% of the time. This causes sizeable back-tracking of the inactive RNAP, on average 59 nm upstream of the promoter. A significant fraction of the collisions (~15%) are between actively transcribing RNAP while the remainder (~11%) are undetermined. End-labelling of dsDNA using nucleic acid structures did not interfere with AFM sample preparation and can be used as a generic approach to studying interactions of multiple proteins on DNA templates at the single molecule level.
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Chammas, Oliver. "Concurrent DNA transcription from convergent and tandem promoters studied by atomic force microscopy." Thesis, University of Leeds, 2016. http://etheses.whiterose.ac.uk/15361/.
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With recent advances in sequencing and mapping of genomes, the occurrence of overlapping and nested transcription units is more common than previously thought in both eukaryotes and prokaryotes. The interleaved genome model means that transcriptional interference by collisions between concurrently transcribing RNA polymerases is more likely than ever before. This thesis presents a study of the outcomes of collisions between RNAPs transcribing concurrently from convergent and tandem promoters using AFM to provide a view of single populations seen after collisions. Through the development of an improved DNA end labelling method and incorporation of an inhibitor of RNAP non-specific binding the results of collisions can be viewed with more confidence than previously possible. It was seen that collisions from both convergent and tandem promoters resulted in both RNAPs remaining bound to the template in hard contact. These collisions occurred by two main mechanisms. Either between two active elongation complexes (ECs) or between an elongation complex and an inactive complex referred to as a sitting duck (SD). EC-EC collisions were found to be the most common for convergent promoters while with tandem promoters the distinction between the two is less clear. In the case of EC-SD collisions it is shown that shunting upstream of up to 100 bp by an EC is possible. By utilizing a linear template that is susceptible to supercoiling due to spin locking, it is shown that a region of highly positive supercoiled domain can prevent two convergently transcribing RNAPS coming into hard contact. It is also shown that topology of the DNA plays a role in the distribution of EC-EC and EC-SD collisions that occur for both promoter arrangements. This indicates that topology influences the outcomes of concurrent transcription and provides a mechanism by which RNAPs can sense one another via the DNA template.
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Croniger, Colleen Marie. "Convergent transcription of the myosin heavy chain gene (Mhc) and transcriptional unit at chromosomal locus 36B (TU-36B) in Drosophila." Case Western Reserve University School of Graduate Studies / OhioLINK, 1992. http://rave.ohiolink.edu/etdc/view?acc_num=case1059654256.
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Deb, Maharshi Krishna. "Generation of antisense RNAs at convergent gene loci in cells undergoing senescence." Thesis, Toulouse 3, 2016. http://www.theses.fr/2016TOU30274.
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La sénescence, qui est un mécanisme antitumoral majeur, est définie comme un état d'arrêt irréversible de la prolifération cellulaire en réponse à un stress comme l'activation illégitime d'oncogènes. Les cellules qui entrent en sénescence subissent de profonds changements de leur épigénome. Les ARNs antisens sont suspectés de joue des rôles importants dans le contrôle du destin cellulaire et dans des processus cellulaires variés. Dans la levure, le variant d'histone H2A.Z co-opère avec les machineries du RNAi et de l'hétérochromatine pour réprimer sur les loci de gènes convergents l'apparition d'antisens dus à des défauts de terminaison de transcription de un des deux gènes. Chez les mammifères, l'existence et la régulation de tels transcrits antisens restent inconnues. De façon intéressante, la déplétion du variant d'histones H2A.Z est connue pour induire la sénescence. Nous nous sommes donc demandés si la sénescence est accompagnée de la régulation de tels transcrits antisens sur les gènes convergents, si la régulation par H2A.Z est conservée et si ces transcrits pouvaient avoir un rôle fonctionnel. Dans un modèle de sénescence induite par les oncogènes in vitro, nous avons identifiés par RNA-Seq brin spécifiques plusieurs loci de gènes convergents où des ARN antisens pourraient être générés par des défauts de terminaison de transcription sur le gène convergent. Des analyses en profondeurs sur deux loci ont confirmé que les transcrits antisens sont effectivement générés par un tel mécanisme (appelé "read-through transcriptionnel"). Nous avons appelé ces antisens START RNAs (pour " Senescence Triggered Antisense Read-through Transcripts). Nous avons par la suite montré que ces STARTs répriment l'expression du gène pour lequel ils sont antisens. Finalement, nous avons montré qu'ils sont réprimés par H2A.Z dans les cellules en prolifération. Nous proposons donc un modèle où la progression en sénescence s'accompagne d'une diminution de H2A.Z, ce qui se traduit par l'induction de transcrits antisens régulateurs sur une famille de loci de gènes convergents dus à des défauts de contrôle de la terminaison de la transcriptionCellular senescence represents one of the major fail-safe mechanisms that counteracts tumour development is defined as a state of irreversible cell cycle arrest as a consequence of stress response such as oncogenic challenge. Such cells undergoing Oncogene-induced Senescence (OIS) display profound alternation in their epigenome as their chromatin are largely decorated with prominent drivers of constitutive heterochromatin.Antisense RNA-mediated gene regulation has been attributed to play diverse roles in mediating various cellular processes and cell fates per-se. In yeast, histone variant H2A.Z cooperates with RNAi and heterochromatin machinery to regulate antisense transcription at convergent gene loci which can otherwise generate pervasive read-through transcripts owing to improper transcription termination. In mammals, whether such antisense transcripts (occurring by read-through transcription at convergent gene pairs) exist and how they are regulated remains unknown. Interestingly, the depletion of the human H2A.Z histone variant has been reported to induce cellular senescence. We thus wondered if the regulation of particular antisense transcripts at convergent gene pairs occurs in senescence, if their regulation by H2A.Z is conserved in mammals and, if so, if a functional significance can be attributed to these transcripts. To this end we took advantage of a well-established in-vitro OIS model. Briefly, we analysed genome wide strand specific RNA-seq analysis of cells undergoing Oncogene Induced Senescence. This led us to identify numerous convergent gene loci associated with accumulation of transcripts downstream of the designated transcription termination site in senescent cells, and extending to generate an antisense to the next gene located in the opposite strand of the convergent gene pair. We confirmed the RNA-seq data at two of such convergent loci. An RNAi based approach revealed that at least two of these transcripts are generated by transcriptional read-throughs. Hence we designated such pervasive transcripts as Senescence Triggered Antisense Read-through Transcripts (START). Importantly, we further found that the two STARTs for which we performed in depth studies repress the expression of the gene for which they are antisense. Finally, we demonstrate that the histone variant H2A.Z suppresses the accumulation of STARTs in proliferative cells. Since it also prevents senescence induction, this suggests that expression of START is important for cellular senescence. This has lead us to propose a model that human cells undergoing OIS are associated with loss of H2A.Z that leads to the wide spread accumulation of read-through transcripts owing to impaired termination control
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Yi, Jia. "The Role of Convergent Transcription in Regulating Alternative Splicing : Targeted Epigenetic Modification via Repurposed CRISPR/Cas9 System and Its Impact on Alternative Splicing Modulation." Electronic Thesis or Diss., Sorbonne université, 2020. http://www.theses.fr/2020SORUS382.
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L'épissage alternatif de l'ARN précurseur est un processus co-transcriptionnel qui affecte la grande majorité des gènes humains et contribue à la diversité des protéines. Le dérèglement d'un tel processus est impliqué dans diverses maladies, y compris la tumorigènes. Cependant, les mécanismes qui régulent ces processus restaient à caractériser. Dans cette étude, nous avons montré que les perturbations de l'épissage alternatif étaient corrélées aux dérèglements de la transcription convergente et de la méthylation de l'ADN. Une transcription convergente peut être générée entre des paires de gènes voisins en en orientation opposée, ou entre des amplificateurs intragéniques et leur gène hôte. CENPO et ADCY3 ont été identifiés comme une paire de gènes de transcription convergentes. Nous avons constaté, dans un modèle de progression tumorale du cancer du sein, que le changement d'épissage de l'exon22 variant d'ADCY3 était corrélé à une augmentation de sa transcription qui allait contre celle de CENPO. En utilisant le système de répression ciblée de la transcription CRISPRi, nous avons démontré que l’inhibition de la transcription de CENPO ne pouvait pas inverser l'altération d'épissage alternatif d'ADCY3 dans les cellules cancéreuses (DCIS). Un activateur intragénique actif a été identifié dans l'intron16 du gène CD44, en aval de ses exons alternatifs. En utilisant le système d'activation ciblée de transcription CRISPRa, nous avons montré que l’augmentation de la transcription de CD44 ne pouvait pas modifier l'épissage alternatif de CD44 dans les cellules DCIS. Ces résultats suggèrent que la modification de transcription convergente par des changements d’activité des promoteurs ne permet pas d’altérer l'épissage alternatif de ADCY3 et CD44 dans les cellules DCIS. Cependant, en remplaçant l'amplificateur intragénique par un promoteur inductible, nous avons constaté que l'activation de la transcription intragénique augmentait le niveau d'inclusion de plusieurs exons alternatifs de CD44 dans les cellules HCT116. Ce résultat suggère que la transcription convergente local pourrait avoir un impact direct sur l'épissage alternatif de CD44. De plus, en utilisant le système de méthylation de l'ADN ciblée CRISPR/dCas9-DNMT3b, nous avons démontré que la méthylation de l'ADN au niveau des exons variants pouvait modifier l'épissage alternatif de CD44. Ce travail de thèse a également exploré les limites et la faisabilité de l'étude de l'épissage alternatif avec des outils moléculaires basés sur le système CRISPRAlternative splicing of precursor RNA is a co-transcriptional process that affects the vast majority of human genes and contributes to protein diversity. Dysregulation of such process is implicated in various diseases, including tumorigenesis. However, the mechanisms regulating these processes were still to be characterized. In this study, we showed that perturbations of alternative splicing correlated with dysregulations of convergent transcription and DNA methylation. Convergent transcription could be generated between pairs of neighboring genes in opposite orientation, or between intragenic enhancers and their host gene. CENPO and ADCY3 was identified as a convergent transcription gene pair. We found, in a tumor progression model of breast cancer, that the splicing change of the ADCY3 variant exon22 correlated with an increase of its transcription that went against that of CENPO. By using targeted transcription repression system CRISPRi, we demonstrated that downregulating the transcription of CENPO could not reverse the alternative splicing alteration of ADCY3 in cancer cells (DCIS). An active intragenic enhancer was identified in the intron16 of CD44, at the downstream of its alternative exons. By using targeted transcription activation system CRISPRa, we showed that upregulating the transcription of CD44 could not alter the alternative splicing of CD44 in DCIS cells. These results suggest that convergent transcription modulation through changes of promoter activity does not alter the alternative splicing of ADCY3 and CD44 in DCIS cells. However, through replacing the intragenic enhancer by an inducible promoter, we found that intragenic transcription activation increased the inclusion level of several alternative exons of CD44 in HCT116 cells. This result suggested that local convergent transcription could have a direct impact on the alternative splicing of CD44. Furthermore, by using targeted DNA methylation system CRISPR/dCas9-DNMT3b, we showed that DNA methylation at variant exons could directly modify CD44 alternative splicing. This thesis work also explored the limitation and feasibility of studying alternative splicing with repurposed CRISPR systems
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Omont, Nicolas Képès François. "La convergence des modularités structurelles et fonctionnelles des systèmes complexes." S. l. : Evry-Val d'Essonne, 2009. http://www.biblio.univ-evry.fr/theses/2008/2008EVRY0037.pdf.
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Ivanova, Tsvetomira Georgieva 1978. "The DNA damage and the DNA synthesis checkpoints converge at the MBF transcription factor." Doctoral thesis, Universitat Pompeu Fabra, 2012. http://hdl.handle.net/10803/116932.
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DNA damage is an ongoing threat to both the ability of the cell to faithfully transmit genetic information to its offspring as well as to its own survival. In order to maintain genomic integrity, eukaryotes have developed a highly conserved mechanism to detect, signal and repair damage in DNA, known as the DNA damage response (DDR). In fission yeast the two DDR pathways converge at the regulation of single transcriptional factor complex (MBF) resulting in opposite directions. We have shown that when the DNA-synthesis checkpoint is activated, Max1 is phosphorylated by Cds1 resulting in the abrogation of its binding to MBF. As a consequence, MBF-dependent transcription is maintained active until cells are able to overcome the replication challenge. In contrast, upon DNA damage, Chk1 the effector kinase of DNA damage checkpoint is activated and blocks the cell cycle progression, inducing DNA repair and repressing the MBF dependent transcription. We have revealed that Cdc10 is the target of the DNA-damage checkpoint and when cells are treated with MMS or are exposed to IR, Chk1 phosphorylates Cdc10 inducing the exit of MBF from chromatin. The consequence is that under these conditions, MBF-dependent transcription is repressed. Thus, Max1 and Cdc10 couple normal cell cycle regulation and the DNA-synthesis and DNA-damage checkpoints into MBF.
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Batlle, Ana. "Regulation of BCL6:p38 MAPK signalling and CTCF transcriptional regulation converge at exon 1." Thesis, Imperial College London, 2010. http://hdl.handle.net/10044/1/6093.
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BCL6 is a zinc finger transcriptional repressor, which is highly expressed in germinal centre B-cells, and is essential for germinal centre formation and T-dependent antibody responses. Deregulated BCL6 expression is associated with certain non- Hodgkin’s lymphomas. High expression is observed in breast cancer. Tight lineage and temporal regulation of BCL6 is, therefore, required for normal immunity and abnormal regulation occurs in cancer. Regulatory mechanisms have been analysed in two settings. Firstly, BCL6 is strongly induced by the tyrosine kinase inhibitor, Imatinib, in chronic myeloid leukaemia lymphoid blast crisis cell lines, and this effect was used in order to study the effects of phospho-protein signalling on BCL6 expression and a major finding is that p38 MAPK induced BCL6. Also, p38 is, at least in part, responsible for BCL6 expression in basal conditions in the germinal centre representative Burkitt’s lymphoma cell lines and that qualitatively different CD40 stimuli can either induce or repress BCL6 expression. Luciferase assays showed that p38 acts at a 300bp sequence immediately 5’ of exon 1, and probably also at more distal sequences. Overall it appears that the balance between positive and negative regulatory controls BCL6 expression with inhibitory signalling pathways being predominant in most circumstances. Focusing on BCL6 exon 1, a binding site for the multifunctional regulator CTCF was identified. CTCF interacts in vitro and in vivo with this sequence. Reduced expression of CTCF in germinal centre cells caused a moderate reduction of BCL6 expression. Finally, although no clear differences were observed in the methylation status of the CTCF binding site on exon 1, a significant enrichment of active histone modifications at this site was observed in BCL6 expressing cells, suggesting that CTCF may have a role in the epigenetic regulation of BCL6.
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Demagny, Hadrien. "Convergence des voies de signalisation wnt, fgf et tgf-beta au niveau des facteurs de transcription smad1 et smad4." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066164/document.
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Mon projet de thèse s’inscrit dans le cadre des études visant à comprendre comment les cellules embryonnaires intègrent les différents signaux auxquels elles sont exposées pour s’engager dans une voie de différenciation définie. Il est plus particulièrement centré sur le rôle des protéines Smad dans ces processus et peut se diviser en deux axes de recherche. Le premier a trait au rôle de Mad (Smad1) dans les interactions entre signaux Wnt (Wg) et BMP chez la drosophile. Nous avons pu démontrer que la forme Mad non phosphorylée par le récepteur BMP se lie au complexe transcriptionnel ß-catenin/dTCF et est requise pour le signal Wnt canonique. La phosphorylation de Mad par le récepteur BMP dirige Mad vers la voie BMP, créant la possibilité d’une compétition entre ces deux classes de signaux. Le second axe de recherche concerne le facteur de transcription Smad4 qui est requis pour la transduction des signaux TGF-ß et BMP. J’ai pu identifier trois sites potentiels de phosphorylation par la kinase GSK3 dans la séquence primaire de Smad4. En utilisant de nombreuses techniques de biochimie, j’ai pu montrer que Smad4 est phosphorylé par la kinase Erk, puis par GSK-3 en réponse à un signal FGF. Lorsque Smad4 est doublement phosphorylé, il est reconnu par une E3-ligase, beta-TrCP, ce qui entraine sa polyubiquitination et sa dégradation. La voie Wnt étant capable d’inhiber GSK-3, j’ai pu montrer que Smad4 est stabilisé par des signaux Wnt. Ce mécanisme augmente la sensibilité des cellules aux signaux TGF-beta lorsqu’elles reçoivent également un signal WntDuring my PhD I studied how cells receive and integrate multiple signals from the extracellular milieu. I focused on Smad proteins and my project can be divided into two parts. My first project was centered on the transcription factor Mad (Smad1) and its requirement for the BMP and Wg pathways. Using a combination of genetic and biochemistry experiments, we showed that Mad is required for Wg signaling both in Tcf reporter gene assays and in vivo in Drosophila. We found that the choice for Mad to transduce Dpp or Wg signals is controlled by C-terminal phosphorylations so that Mad binds to Pangolin and participates in Wg target genes transcription only when not phosphorylated at its C-terminus. This results in a competition between Dpp and Wg controlled by the phosphorylation state of Mad. My second project was focused on the tumor suppressor Smad4. When I first joined the lab, I identified three new potential GSK3 phosphorylation sites in Smad4 primary sequence. I used a home-made phospho-specific antibody to demonstrate that FGF or EGF stimulation trigger Erk-mediated phosphorylation of Smad4 which primes subsequent GSK3 phosphorylations. These phosphorylations regulate a transcription activation domain located in Smad4 linker region and generate a Wnt-regulated phosphodegron recognized by the E3 ligase beta-TrCP. This mechanism provides a means of integrating distinct pathways which would otherwise remain insulated, allowing cells to sense FGF and Wnt inputs and adapt TGF-beta outcome to their context. It provides a molecular explanation of the long-standing mystery of the “competence modifier” effect of Wnt on Nodal signals discovered 20 years ago
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Demagny, Hadrien. "Convergence des voies de signalisation wnt, fgf et tgf-beta au niveau des facteurs de transcription smad1 et smad4." Electronic Thesis or Diss., Paris 6, 2014. http://www.theses.fr/2014PA066164.
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Mon projet de thèse s’inscrit dans le cadre des études visant à comprendre comment les cellules embryonnaires intègrent les différents signaux auxquels elles sont exposées pour s’engager dans une voie de différenciation définie. Il est plus particulièrement centré sur le rôle des protéines Smad dans ces processus et peut se diviser en deux axes de recherche. Le premier a trait au rôle de Mad (Smad1) dans les interactions entre signaux Wnt (Wg) et BMP chez la drosophile. Nous avons pu démontrer que la forme Mad non phosphorylée par le récepteur BMP se lie au complexe transcriptionnel ß-catenin/dTCF et est requise pour le signal Wnt canonique. La phosphorylation de Mad par le récepteur BMP dirige Mad vers la voie BMP, créant la possibilité d’une compétition entre ces deux classes de signaux. Le second axe de recherche concerne le facteur de transcription Smad4 qui est requis pour la transduction des signaux TGF-ß et BMP. J’ai pu identifier trois sites potentiels de phosphorylation par la kinase GSK3 dans la séquence primaire de Smad4. En utilisant de nombreuses techniques de biochimie, j’ai pu montrer que Smad4 est phosphorylé par la kinase Erk, puis par GSK-3 en réponse à un signal FGF. Lorsque Smad4 est doublement phosphorylé, il est reconnu par une E3-ligase, beta-TrCP, ce qui entraine sa polyubiquitination et sa dégradation. La voie Wnt étant capable d’inhiber GSK-3, j’ai pu montrer que Smad4 est stabilisé par des signaux Wnt. Ce mécanisme augmente la sensibilité des cellules aux signaux TGF-beta lorsqu’elles reçoivent également un signal WntDuring my PhD I studied how cells receive and integrate multiple signals from the extracellular milieu. I focused on Smad proteins and my project can be divided into two parts. My first project was centered on the transcription factor Mad (Smad1) and its requirement for the BMP and Wg pathways. Using a combination of genetic and biochemistry experiments, we showed that Mad is required for Wg signaling both in Tcf reporter gene assays and in vivo in Drosophila. We found that the choice for Mad to transduce Dpp or Wg signals is controlled by C-terminal phosphorylations so that Mad binds to Pangolin and participates in Wg target genes transcription only when not phosphorylated at its C-terminus. This results in a competition between Dpp and Wg controlled by the phosphorylation state of Mad. My second project was focused on the tumor suppressor Smad4. When I first joined the lab, I identified three new potential GSK3 phosphorylation sites in Smad4 primary sequence. I used a home-made phospho-specific antibody to demonstrate that FGF or EGF stimulation trigger Erk-mediated phosphorylation of Smad4 which primes subsequent GSK3 phosphorylations. These phosphorylations regulate a transcription activation domain located in Smad4 linker region and generate a Wnt-regulated phosphodegron recognized by the E3 ligase beta-TrCP. This mechanism provides a means of integrating distinct pathways which would otherwise remain insulated, allowing cells to sense FGF and Wnt inputs and adapt TGF-beta outcome to their context. It provides a molecular explanation of the long-standing mystery of the “competence modifier” effect of Wnt on Nodal signals discovered 20 years ago
Books on the topic "Convergent transcription"
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Campione, Marina, Amelia Aranega, and Diego Franco. Cardiac looping and laterality. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0014.
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Dextral looping is a complex process which progresses concomitantly with cardiac chamber differentiation and ultimately leads to the final alignment of the cardiac regions. Generation of cardiac asymmetry is crucial to ensure the proper form and consequent function of the heart and thus is a highly regulated process. Molecular signals originate long before morphological asymmetry and therefore can direct it; a complex regulatory network has been characterized which invariably converges on the Tgf-β signalling molecule Nodal and its downstream target, the homeobox transcription factor Pitx2. We review current data regarding the cellular and molecular bases of cardiac looping and laterality, and describe current understaning of the role of Nodal and Pitx2. The morphogenetic role of the Pitx2 gene and its modulation of transcription and function, which have recently linked laterality to atrial fibrillation, are emphasized.
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Miquerol, Lucile. Origin and development of the cardiac conduction system. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0015.
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The cardiac conduction system represents the ‘wiring’ of the heart and orchestrates the propagation of the electrical activity to synchronize heartbeats. It is built from specialized cardiomyocytes expressing a subset of ion channels and gap junctions indispensable for their electrophysiological properties. Although representing only a very small volume of the heart, the conduction system plays a crucial role in the appearance of cardiac arrhythmias. The cells forming the conduction system are derived from the same cardiac progenitors as the working cardiomyocytes, and the choice between these two fates is acquired during embryonic development. The components of the conduction system are progressively established during cardiac morphogenesis and converge to form an integrated electrical system in the definitive heart. This chapter will discuss recent advances using mouse genetic approaches which have improved understanding of the cellular origin and the transcriptional regulatory networks involved in the development of the conduction system.
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Fiddes, Paul S. Charles Williams and C. S. Lewis. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780192845467.001.0001.
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This study of the literary relationship between Charles Williams and C. S. Lewis during the years 1936–1945 focuses on the theme of ‘co-inherence’ at the centre of their friendship. The idea of co-inherence has long been recognized as an important contribution of Williams to theology, and had significant influence on the thought of Lewis. This account of the two writers’ conviction that human persons ‘inhere’ or dwell both in each other and in the triune God reveals many interrelationships between their writings that would otherwise be missed. It also shows up profound differences between their world views, and a gradual, though incomplete, convergence onto common ground. Exploring the idea of co-inherence throws light on the fictional worlds they created, as well as on their treatment (whether together or separately) of a wide range of theological and literary subjects: the Arthurian tradition, the poetry of William Blake and Thomas Traherne, the theology of Karl Barth, the nature of human and divine love, and the doctrine of the Trinity. This study draws for the first time on transcriptions of Williams’ lectures from 1932 to 1939, tracing more clearly the development and use of the idea of co-inherence in his thought than has been possible before. Finally, an account of the use of the word ‘co-inherence’ in English-speaking theology suggests that the differences between Lewis and Williams, especially on the place of analogy and participation in the human experience of God, might be resolved by a theology of co-inherence in the Trinity.
Book chapters on the topic "Convergent transcription"
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Kwak, Sun-Dong, and Moon-Soo Chang. "Development of Transcription Tools That Improved Safety and Convenience." In Convergence and Hybrid Information Technology, 294–301. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-32692-9_38.
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Giglio, Lorenzo. "Ancora su Boccaccio copista di Dante: (almeno) tre ‘redazioni’ della Vita nuova." In Intorno a Boccaccio / Boccaccio e dintorni 2020, 23–38. Florence: Firenze University Press, 2021. http://dx.doi.org/10.36253/978-88-5518-510-3.03.
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The paper studies the editorial practice of Boccaccio in his copies of Dante’s Vita Nuova, through a textual comparison between the two preserved transcriptions and the ones that are only hypothetically referable to his work, thanks to an examination of the varia lectio. What emerged for Vita Nuova from a new comprehensive collatio of the most important witnesses of Boccaccio’s manuscript tradition, put together with what is known about the other Dante’s works copied by Boccaccio himself (lyrics and Commedia), seem to converge in the hypothesis, already suggested by Michele Barbi, that around the interpositus b3 it is quite recognizable a third “authorial edition”, originally conceived like the other two, and perhaps currently surviving in the manuscript Riccardiano 1035.
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Dwivedi, Nidhi, Vinay Kumar, and Jitendra K. Thakur. "Convergence of Stress-Induced Hormone Signaling Pathways on a Transcriptional Co-Factor." In Mechanism of Plant Hormone Signaling under Stress, 285–317. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781118889022.ch28.
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Seligmann, Herve. "Mutation Patterns Due to Converging Mitochondrial Replication and Transcription Increase Lifespan, and Cause Growth Rate-Longevity Tradeoffs." In DNA Replication-Current Advances. InTech, 2011. http://dx.doi.org/10.5772/24319.
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Ellison, Jay w. "SHOX and Dyschondrosteosis and Turner Syndrome." In Inborn Errors Of Development, 735–39. Oxford University PressNew York, NY, 2008. http://dx.doi.org/10.1093/oso/9780195306910.003.0077.
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Abstract The story of the short stature homeobox (SHOX) gene is an example of how observations of different clinical disorders can eventually converge on a single gene. The disorders in this case are dyschondrosteosis, a skeletal dysplasia; Turner syndrome, an aneuploid condition resulting from a missing sex chromosome; and idiopathic short stature (ISS). SHOX is implicated in each of these conditions, although its contribution to the phenotypes varies with respect to both level of involvement and level of experimental proof. The predicted nature of the gene product (as a DNA-binding transcriptional regulator), its abundant expression in bone, and the skeletal phenotypes of patients all point to the placement of SHOX in a developmental pathway of bone development. Details of this pathway are largely unknown, though preliminary studies suggest that SHOX may be important for proper chondrocyte differentiation in the relevant skeletal elements. This notion is supported by observations of a conditional knockout model of a mouse SHOX paralog (Shox2). Functional studies of SHOX have centered on in vitro systems that have identified functional domains of the SHOX gene, messenger RNA (mRNA), and protein. In addition, a cis-regulatory element has been inferred on the basis of deletions in a subset of patients. Continued work on these and other fronts will eventually lead to a better understanding of the role of SHOX in growth and skeletal development.
Conference papers on the topic "Convergent transcription"
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Sonawane, Dayaram, Manan Pathak, and Venkat R. Subramanian. "Convergence rates for direct transcription of optimal control problems using Second Derivative Methods." In 2016 American Control Conference (ACC). IEEE, 2016. http://dx.doi.org/10.1109/acc.2016.7524918.
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Bang, Jeong-Uk, Sang-Hun Kim, and Oh-Wook Kwon. "Phoneme Set Extension Based on Jensen-Shannon Divergence for Broadcast News Transcription." In 2020 International Conference on Information and Communication Technology Convergence (ICTC). IEEE, 2020. http://dx.doi.org/10.1109/ictc49870.2020.9289468.
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Sophea, Seng, and Somnuk Phon-Amnuaisuk. "Determining a Suitable Desired Factors for Nonnegative Matrix Factorization in Polyphonic Music Transcription." In 2007 International Symposium on Information Technology Convergence (ISITC 2007). IEEE, 2007. http://dx.doi.org/10.1109/isitc.2007.50.
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You, Yeonguk, Hyangrae Noh, Jaeeun Park, Yunsoo Kim, Yongjin KwaK, and Yoonjoong Kim. "A development of a speech data transcription tool for building a spoken corpus." In 2018 International Conference on Information and Communication Technology Convergence (ICTC). IEEE, 2018. http://dx.doi.org/10.1109/ictc.2018.8539450.
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Sunkel, Benjamin D., Dayong Wu, Xiangtao Liu, Zhenqing Ye, Victor Jin, and Qianben Wang. "Abstract 1387: Convergent CREB1/FoxA1 transcriptional activity defines castration-resistant prostate cancer gene expression profile." 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.am2014-1387.
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Karneswaran, S., and L. T. Biegler. "Convergence rates for direct transcription of optimal control problems with final-time equality constraints using collocation at Radau points." In 2006 American Control Conference. IEEE, 2006. http://dx.doi.org/10.1109/acc.2006.1655348.
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Bodin, Per, Kristian Lindqvist, David Seelbinder, Artemi Makarow, José Garrido, Alessandro Visintini, Marilena Di Carlo, Andrew Hyslop, and Valentin Preda. "Attitude Guidance Using On-Board Optimisation." In ESA 12th International Conference on Guidance Navigation and Control and 9th International Conference on Astrodynamics Tools and Techniques. ESA, 2023. http://dx.doi.org/10.5270/esa-gnc-icatt-2023-113.
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The on-board ability to autonomously plan and execute constrained attitude manoeuvres is expected to play an important role in many future space missions. The work presented in this paper summarizes the results from a recently completed ESA study in which such functionality was examined. The study included the application of on-board embedded optimisation techniques to solve constrained attitude guidance problems. Different heritage methods not based on on-board optimisation were also developed and applied for comparison. The study demonstrated the capabilities in a number of test cases associated with two benchmark problems based on the Comet Interceptor and Theseus mission studies. The performance was examined within Monte Carlo simulations as well as within execution on a ZedBoard hardware platform. The use of numerical optimisation has experienced a huge acceleration over the last years. Convex optimisation is appealing mainly since the local optimum is also the global optimum and since very efficient general-purpose and highly dedicated solvers exist. In addition, the dependency on initial guesses is completely lifted. Convex optimisation methods are flexible enough to permit the modelling of a huge number of problems of practical interest. A particularly successful category of problems, the Second-Order Cone Programming (SOCP) problem is a generalization of quadratic programming that includes the possibility of embedding conic constraints in the formulation. This type of formulation has been widely used in many fields, and with particular success in GNC, especially for guidance applications such as powered-descent and landing, and atmospheric re-entry. More notably, this technology has been successfully employed on several rockets and vehicles, including the Falcon 9 and the experimental DLR vehicle EAGLE. Resulting from a trade-off performed in the study, the selected baseline strategy was to combine second-order cone programming (SOCP) with successive convexification into sequential convex programming (SCVX), inspired by the work of Mao and Bonalli. The SOCP problem class perfectly fits the constraints required to model the benchmark scenarios and the DLR experience in using similar methods for vertical takeoff and landing (VTVL) vehicles demonstrates, that it is a reliable, fast convergent method. A pseudospectral discretization method was selected based on prior experience. The heritage methods applied for the Comet Interceptor benchmark case was based on simplified slew strategies parameterized by a reduced parameter set. The solution is obtained numerically taking into account the numerical evolution of the nominal angular and rate profiles. An eigenaxis slew algorithm was chosen for Theseus as a result of a trade-off with alternative heritage guidance methods including artificial potential functions and path planning algorithms, where these methods were rejected due to lack of convergence guarantee and because of their computational complexity. For the Comet Interceptor benchmark cases, the results from the Monte Carlo simulations demonstrate that for the more nominal cases, the results from using the SCVX and heritages solutions are comparable in terms of minimising the time the target object is outside of the field-of-view of the payload instruments. For the contingency cases, the SCVX is clearly better than the heritage solution. For Theseus, the slew times resulting from the SCVX solutions are in general shorter than those obtained from the heritage solution. In addition to the Monte Carlo simulations performed for the benchmark cases, the optimisation algorithms were executed on an ARM-Cortex-based development board (ZedBoard), which is supported by the MATLAB Embedded Coder for C code applications. As the SOCP solver is written in C++ it was not possible to rely on the native support. The following procedure was used to facilitate runtime tests: The Embedded Coder was used to generate code of the SCVX algorithm for the ARM-Cortex architecture, including the loading and reading process of the transcription data. Then the GCC cross-compiler was used to build a standalone executable which was uploaded to the ZedBoard. Several conclusions can be drawn from the work performed in the study with in particular the following main areas are of interest: The performance observed from the SCVX based guidance is in most of the test cases better than the guidance resulting from the heritage solutions. The execution times observed from the tests on the flight like HW are in the range of 30 to 40 s which does not really allow for fast recomputation of the guidance profiles in connection with critical re-configuration of HW or in other cases, where the guidance profile is needed quickly. It is however expected that there is some room for improvement in terms of execution time. An estimate of development effort shows that the application-specific required, recurrent effort is similar for the development of the optimisation-based and the heritage solutions. However, the optimisation-based solution also requires a significant initial, non-recurring effort to develop the necessary numeric optimisation software. This is estimated to be about 5 times as much as the effort for a single mission application, not counting the development of the core convex solver. The observations and conclusions summarized above indicate that choosing an SCVX-based attitude guidance solution is not a “magic” universal tool that seamlessly will solve any problem. Significant effort is needed to be able to arrive at a well-posed and well-tuned problem that allows the optimisation-based framework to provide a solution. However, with such a problem at hand, the framework is able to provide a versatile solution that seems to be able to better utilize the on-board resources and deliver a solution that provides better performance than the heritage approach.
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Cuiffo, Benjamin, Antoine Campagne, George W. Bell, Evan Lien, Manoj K. Bhasin, Odette Mariani, Anne Vincent-Salomon, and Antoine Karnoub. "Abstract 173: Tumor proximal mesenchymal stem cells initiate a pro-metastatic microRNA regulatory network which acts via convergent targeting of the speech-associated transcriptional repressor FOXP2." 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.am2014-173.
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Garg, Rachana, Jorge Blando, Carlos Perez, Martin Abba, Fernando Benavides, and Marcelo Kazanietz. "Abstract LB-230: Oncogenic PKC epsilon and Pten loss converge on activating CXCL13 via atypical NF-κB transcriptional signaling in prostate cancer progression." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-lb-230.
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Linher-Melville, K., MG Nashed, R. Ungard, S. Haftchenary, PT Gunning, and G. Singh. "Abstract P3-03-13: Chronic inhibition of signal transducer and activator of transcription 3/5 in treatment-resistant human breast cancer cell subtypes: Convergence on the reactive oxyten species/SUMOylation pathway and its effects on xCT expression and system xc-activity." In Abstracts: 2016 San Antonio Breast Cancer Symposium; December 6-10, 2016; San Antonio, Texas. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.sabcs16-p3-03-13.
Full textReports on the topic "Convergent transcription"
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Levy, Avraham A., and Virginia Walbot. Regulation of Transposable Element Activities during Plant Development. United States Department of Agriculture, August 1992. http://dx.doi.org/10.32747/1992.7568091.bard.
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We have studied the regulation of the maize Ac and MuDR transposable elements activities during plant development. Ac was studied in an heterologous system (transgenic tobacco plants and cell suspensions) while MuDR was studied in the native maize background. The focus of this study was on the transcriptional regulation of Ac and MuDR. For Ac, the major achievements were to show that 1-It is autoregulated in a way that the Ac-encoded transposase can repress the activity of its own promoter; 2-It is expressed at low basal level in all the plant organs that were studied, and its activity is stronger in dividing tissues -- a behaviour reminiscent of housekeeping genes; 3- the activity of Ac promoter is cell cycle regulated -- induced at early S-phase and increasing until mitosis; 4- host factor binding sites were identified at both extremities of Ac and may be important for transposition. For MuDR, It was shown that it encodes two genes, mudrA and mudrB, convergently transcribed from near-identical promoters in the terminal inverted repeats. Distinct 5' start sites, alternative splicing, production of antisense RNA and tissue specificity were all shown to be involved in the regulation of MuDR.
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Samach, Alon, Douglas Cook, and Jaime Kigel. Molecular mechanisms of plant reproductive adaptation to aridity gradients. United States Department of Agriculture, January 2008. http://dx.doi.org/10.32747/2008.7696513.bard.
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Annual plants have developed a range of different mechanisms to avoid flowering (exposure of reproductive organs to the environment) under adverse environmental conditions. Seasonal environmental events such as gradual changes in day length and temperature affect the timing of transition to flowering in many annual and perennial plants. Research in Arabidopsis and additional species suggest that some environmental signals converge on transcriptional regulation of common floral integrators such as FLOWERING LOCUS T (FT). Here we studied environmental induction of flowering in the model legume Medicago truncatula. Similarly to Arabidopsis, the transition to flowering in M. truncatula is hastened by long photoperiods and long periods of vernalization (4°C for 2-3 weeks). Ecotypes collected in Israel retain a vernalization response even though winter temperatures are way above 4°C. Here we show that this species is also highly responsive (flowers earlier) to mild ambient temperatures up to 19°C simulating winter conditions in its natural habitat. Physiological experiments allowed us to time the transition to flowering due to low temperatures, and to compare it to vernalization. We have made use of natural variation, and induced mutants to identify key genes involved in this process, and we provide here data suggesting that an FT gene in M.truncatula is transcriptionally regulated by different environmental cues. Flowering time was found to be correlated with MtFTA and MtFTB expression levels. Mutation in the MtFTA gene showed a late flowering phenotype, while over-expressing MtFTA in Arabidopsis complemented the ft- phenotype. We found that combination of 4°C and 12°C resulted in a synergistic increase in MtFTB expression, while combining 4°C and long photoperiods caused a synergistic increase in MtFTA expression. These results suggest that the two vernalization temperatures work through distinct mechanisms. The early flowering kalil mutant expressed higher levels of MtFTA and not MtFTB suggesting that the KALIL protein represses MtFTA specifically. The desert ecotype Sde Boker flowers earlier in response to short treatments of 8-12oc vernalization and expresses higher levels of MtFTA. This suggests a possible mechanism this desert ecotype developed to flower as fast as possible and finish its growth cycle before the dry period. MtFTA and FT expression are induced by common environmental cues in each species, and expression is repressed under short days. Replacing FT with the MtFTA gene (including regulatory elements) caused high MtFTA expression and early flowering under short days suggesting that the mechanism used to repress flowering under short days has diversified between the two species.The circadian regulated gene, GIGANTEA (GI) encodes a unique protein in Arabidopsis that is involved in flowering mechanism. In this research we characterized how the expression of the M.truncatula GI ortholog is regulated by light and temperature in comparison to its regulation in Arabidopsis. In Arabidopsis GI was found to be involved in temperature compensation to the clock. In addition, GI was found to be involved in mediating the effect of temperature on flowering time. We tested the influence of cold temperature on the MtGI gene in M.truncatula and found correlation between MtGI levels and extended periods of 12°C treatment. MtGI elevation that was found mostly after plants were removed from the cold influence preceded the induction of MtFT expression. This data suggests that MtGI might be involved in 12°C cold perception with respect to flowering in M.truncatula. GI seems to integrate diverse environmental inputs and translates them to the proper physiological and developmental outputs, acting through several different pathways. These research enabled to correlate between temperature and circadian clock in M.truncatula and achieved a better understanding of the flowering mechanism of this species.