Journal articles: 'Convergent transcription'

1

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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10

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.

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11

El Houdaigui, Bilal, Raphaël Forquet, Thomas Hindré, Dominique Schneider, William Nasser, Sylvie Reverchon, and Sam Meyer. "Bacterial genome architecture shapes global transcriptional regulation by DNA supercoiling." Nucleic Acids Research 47, no. 11 (April 24, 2019): 5648–57. http://dx.doi.org/10.1093/nar/gkz300.

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Abstract DNA supercoiling acts as a global transcriptional regulator in bacteria, that plays an important role in adapting their expression programme to environmental changes, but for which no quantitative or even qualitative regulatory model is available. Here, we focus on spatial supercoiling heterogeneities caused by the transcription process itself, which strongly contribute to this regulation mode. We propose a new mechanistic modeling of the transcription-supercoiling dynamical coupling along a genome, which allows simulating and quantitatively reproducing in vitro and in vivo transcription assays, and highlights the role of genes’ local orientation in their supercoiling sensitivity. Consistently with predictions, we show that chromosomal relaxation artificially induced by gyrase inhibitors selectively activates convergent genes in several enterobacteria, while conversely, an increase in DNA supercoiling naturally selected in a long-term evolution experiment with Escherichia coli favours divergent genes. Simulations show that these global expression responses to changes in DNA supercoiling result from fundamental mechanical constraints imposed by transcription, independently from more specific regulation of each promoter. These constraints underpin a significant and predictable contribution to the complex rules by which bacteria use DNA supercoiling as a global but fine-tuned transcriptional regulator.

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12

Tripathi, Shubham, Sumitabha Brahmachari, José N. Onuchic, and Herbert Levine. "DNA supercoiling-mediated collective behavior of co-transcribing RNA polymerases." Nucleic Acids Research 50, no. 3 (December 24, 2021): 1269–79. http://dx.doi.org/10.1093/nar/gkab1252.

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Abstract Multiple RNA polymerases (RNAPs) transcribing a gene have been known to exhibit collective group behavior, causing the transcription elongation rate to increase with the rate of transcription initiation. Such behavior has long been believed to be driven by a physical interaction or ‘push’ between closely spaced RNAPs. However, recent studies have posited that RNAPs separated by longer distances may cooperate by modifying the DNA segment under transcription. Here, we present a theoretical model incorporating the mechanical coupling between RNAP translocation and the DNA torsional response. Using stochastic simulations, we demonstrate DNA supercoiling-mediated long-range cooperation between co-transcribing RNAPs. We find that inhibiting transcription initiation can slow down the already recruited RNAPs, in agreement with recent experimental observations, and predict that the average transcription elongation rate varies non-monotonically with the rate of transcription initiation. We further show that while RNAPs transcribing neighboring genes oriented in tandem can cooperate, those transcribing genes in divergent or convergent orientations can act antagonistically, and that such behavior holds over a large range of intergenic separations. Our model makes testable predictions, revealing how the mechanical interplay between RNAPs and the DNA they transcribe can govern transcriptional dynamics.

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Castilla-Earls, Anny, and Katrina Fulcher-Rood. "Convergent and Divergent Validity of the Grammaticality and Utterance Length Instrument." Journal of Speech, Language, and Hearing Research 61, no. 1 (January 22, 2018): 120–29. http://dx.doi.org/10.1044/2017_jslhr-l-17-0152.

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Purpose This feasibility study examines the convergent and divergent validity of the Grammaticality and Utterance Length Instrument (GLi), a tool designed to assess the grammaticality and average utterance length of a child's prerecorded story retell. Method Three raters used the GLi to rate audio-recorded story retells from 100 English-speaking preschool children. To examine convergent validity, the results of the GLi were correlated with 2 language sample measures, mean length of utterance in words and percentage of grammatical utterances, and with the results of the Structured Photographic Expressive Language Test–Third Edition (Dawson, Stout, & Eyer, 2003). To examine divergent validity, the results of the GLi were correlated with the results of the Kaufman Brief Intelligence Test–Second Edition (Kaufman & Kaufman, 2004). Comparisons between task completion time for the GLi and Systematic Analysis of Language Transcripts (SALT; Miller & Iglesias, 2010) transcription and analysis were also conducted. Last, preliminary discriminant analysis was used to examine the diagnostic potential of the GLi. Results The results of this study provide evidence of convergent and divergent validity for the GLi. The task completion time for the GLi was considerably shorter than the SALT transcription and analysis. Preliminary analysis of diagnostic accuracy suggests that the GLi has the potential to be a good tool to identify children with language impairment. Discussion The GLi has good convergent and divergent validity and is a reliable instrument to assess utterance length and grammaticality of prerecorded language samples. However, SALT transcription and analysis provide a more detailed and comprehensive analysis of the language skills of a child.

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14

Meng, Fei-Long, Zhou Du, Alexander Federation, Jiazhi Hu, Qiao Wang, Kyong-Rim Kieffer-Kwon, Robin M. Meyers, et al. "Convergent Transcription at Intragenic Super-Enhancers Targets AID-Initiated Genomic Instability." Cell 159, no. 7 (December 2014): 1538–48. http://dx.doi.org/10.1016/j.cell.2014.11.014.

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15

Pannunzio, Nicholas R., and Michael R. Lieber. "Dissecting the Roles of Divergent and Convergent Transcription in Chromosome Instability." Cell Reports 14, no. 5 (February 2016): 1025–31. http://dx.doi.org/10.1016/j.celrep.2015.12.098.

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16

Iosue, Christine L., Anthony P. Gulotta, Kathleen B. Selhorst, Alison C. Mody, Kristin M. Barbour, Meredith J. Marcotte, Lilian N. Bui, et al. "A Novel cis Element Achieves the Same Solution as an Ancestral cis Element During Thiamine Starvation in Candida glabrata." G3: Genes|Genomes|Genetics 10, no. 1 (November 15, 2019): 321–31. http://dx.doi.org/10.1534/g3.119.400897.

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Regulatory networks often converge on very similar cis sequences to drive transcriptional programs due to constraints on what transcription factors are present. To determine the role of constraint loss on cis element evolution, we examined the recent appearance of a thiamine starvation regulated promoter in Candida glabrata. This species lacks the ancestral transcription factor Thi2, but still has the transcription factor Pdc2, which regulates thiamine starvation genes, allowing us to determine the effect of constraint change on a new promoter. We identified two different cis elements in C. glabrata - one present in the evolutionarily recent gene called CgPMU3, and the other element present in the other thiamine (THI) regulated genes. Reciprocal swaps of the cis elements and incorporation of the S. cerevisiaeThi2 transcription factor-binding site into these promoters demonstrate that the two elements are functionally different from one another. Thus, this loss of an imposed constraint on promoter function has generated a novel cis sequence, suggesting that loss of trans constraints can generate a non-convergent pathway with the same output.

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17

Giordano, Ennio, Rosaria Rendina, Ivana Peluso, and Maria Furia. "RNAi Triggered by Symmetrically Transcribed Transgenes in Drosophila melanogaster." Genetics 160, no. 2 (February 1, 2002): 637–48. http://dx.doi.org/10.1093/genetics/160.2.637.

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Abstract Specific silencing of target genes can be induced in a variety of organisms by providing homologous double-stranded RNA molecules. In vivo, these molecules can be generated either by transcription of sequences having an inverted-repeat (IR) configuration or by simultaneous transcription of sense-antisense strands. Since IR constructs are difficult to prepare and can stimulate genomic rearrangements, we investigated the silencing potential of symmetrically transcribed sequences. We report that Drosophila transgenes whose sense-antisense transcription was driven by two convergent arrays of Gal4-dependent UAS sequences can induce specific, dominant, and heritable repression of target genes. This effect is not dependent on a mechanism based on homology-dependent DNA/DNA interactions, but is directly triggered by transcriptional activation and is accompanied by specific depletion of the endogenous target RNA. Tissue-specific induction of these transgenes restricts the target gene silencing to selected body domains, and spreading phenomena described in other cases of post-transcriptional gene silencing (PTGS) were not observed. In addition to providing an additional tool useful for Drosophila functional genomic analysis, these results add further strength to the view that events of sense-antisense transcription may readily account for some, if not all, PTGS-cosuppression phenomena and can potentially play a relevant role in gene regulation.

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Anderson, Kevin M., Meghan A. Collins, Ru Kong, Kacey Fang, Jingwei Li, Tong He, Adam M. Chekroud, B. T. Thomas Yeo, and Avram J. Holmes. "Convergent molecular, cellular, and cortical neuroimaging signatures of major depressive disorder." Proceedings of the National Academy of Sciences 117, no. 40 (September 21, 2020): 25138–49. http://dx.doi.org/10.1073/pnas.2008004117.

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Major depressive disorder emerges from the complex interactions of biological systems that span genes and molecules through cells, networks, and behavior. Establishing how neurobiological processes coalesce to contribute to depression requires a multiscale approach, encompassing measures of brain structure and function as well as genetic and cell-specific transcriptional data. Here, we examine anatomical (cortical thickness) and functional (functional variability, global brain connectivity) correlates of depression and negative affect across three population-imaging datasets: UK Biobank, Brain Genomics Superstruct Project, and Enhancing NeuroImaging through Meta Analysis (ENIGMA; combined n ≥ 23,723). Integrative analyses incorporate measures of cortical gene expression, postmortem patient transcriptional data, depression genome-wide association study (GWAS), and single-cell gene transcription. Neuroimaging correlates of depression and negative affect were consistent across three independent datasets. Linking ex vivo gene down-regulation with in vivo neuroimaging, we find that transcriptional correlates of depression imaging phenotypes track gene down-regulation in postmortem cortical samples of patients with depression. Integrated analysis of single-cell and Allen Human Brain Atlas expression data reveal somatostatin interneurons and astrocytes to be consistent cell associates of depression, through both in vivo imaging and ex vivo cortical gene dysregulation. Providing converging evidence for these observations, GWAS-derived polygenic risk for depression was enriched for genes expressed in interneurons, but not glia. Underscoring the translational potential of multiscale approaches, the transcriptional correlates of depression-linked brain function and structure were enriched for disorder-relevant molecular pathways. These findings bridge levels to connect specific genes, cell classes, and biological pathways to in vivo imaging correlates of depression.

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Tsaneva-Atanasova, Krasimira, Petros Mina, Christopher J. Caunt, Stephen P. Armstrong, and Craig A. McArdle. "Decoding GnRH neurohormone pulse frequency by convergent signalling modules." Journal of The Royal Society Interface 9, no. 66 (June 15, 2011): 170–82. http://dx.doi.org/10.1098/rsif.2011.0215.

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Gonadotropin-releasing hormone (GnRH) mediates control of reproduction. It is secreted in pulses and acts via intracellular effectors to activate gonadotrophin secretion and gene expression. Sub-maximal GnRH pulse frequency can elicit maximal responses, yielding bell-shaped frequency–response curves characteristic of genuine frequency decoders. GnRH frequency decoding is therapeutically important (pulsatile GnRH can drive ovulation in assisted reproduction whereas sustained activation can treat breast and prostate cancers), but the mechanisms are unknown. Here, we consider the possibility that it is due to convergence of distinct pulsatile signals at the transcriptome. We develop a model that mirrors wet-laboratory data for activation and nuclear translocation of GnRH effectors (extracellular signal regulated kinase and nuclear factors of activated T-cells) and incorporates transcription. The model predicts genuine frequency decoding when two transcription factors (TFs) converge at a cooperative gate, and shows how optimal pulse frequency could reflect TF activation kinetics and affinities. Importantly, this behaviour is revealed as an emergent feature of the network, rather than an intrinsic feature of a given protein or pathway, and since such network topology is extremely common, may well be widespread in biological systems.

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Kim, Dong Eun, Maria-Giuseppina Procopio, Soumitra Ghosh, Seung-Hee Jo, Sandro Goruppi, Francesco Magliozzi, Pino Bordignon, Victor Neel, Paolo Angelino, and G. Paolo Dotto. "Convergent roles of ATF3 and CSL in chromatin control of cancer-associated fibroblast activation." Journal of Experimental Medicine 214, no. 8 (July 6, 2017): 2349–68. http://dx.doi.org/10.1084/jem.20170724.

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Cancer-associated fibroblasts (CAFs) are important for tumor initiation and promotion. CSL, a transcriptional repressor and Notch mediator, suppresses CAF activation. Like CSL, ATF3, a stress-responsive transcriptional repressor, is down-modulated in skin cancer stromal cells, and Atf3 knockout mice develop aggressive chemically induced skin tumors with enhanced CAF activation. Even at low basal levels, ATF3 converges with CSL in global chromatin control, binding to few genomic sites at a large distance from target genes. Consistent with this mode of regulation, deletion of one such site 2 Mb upstream of IL6 induces expression of the gene. Observed changes are of translational significance, as bromodomain and extra-terminal (BET) inhibitors, unlinking activated chromatin from basic transcription, counteract the effects of ATF3 or CSL loss on global gene expression and suppress CAF tumor-promoting properties in an in vivo model of squamous cancer–stromal cell expansion. Thus, ATF3 converges with CSL in negative control of CAF activation with epigenetic changes amenable to cancer- and stroma-focused intervention.

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Lengronne, Armelle, Yuki Katou, Saori Mori, Shihori Yokobayashi, Gavin P. Kelly, Takehiko Itoh, Yoshinori Watanabe, Katsuhiko Shirahige, and Frank Uhlmann. "Cohesin relocation from sites of chromosomal loading to places of convergent transcription." Nature 430, no. 6999 (June 30, 2004): 573–78. http://dx.doi.org/10.1038/nature02742.

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Xue, Peng, David Corbett, Marie Goldrick, Clare Naylor, and Ian S. Roberts. "Regulation of Expression of the Region 3 Promoter of the Escherichia coli K5 Capsule Gene Cluster Involves H-NS, SlyA, and a Large 5′ Untranslated Region." Journal of Bacteriology 191, no. 6 (December 29, 2008): 1838–46. http://dx.doi.org/10.1128/jb.01388-08.

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ABSTRACT Escherichia coli group 2 capsule gene clusters are temperature regulated, being expressed at 37°C but not at 20°C. Expression is regulated at the level of transcription by two convergent promoters, PR1 and PR3. In this paper, we show that regulation of transcription from PR3 involves a number of novel features including H-NS, SlyA, and a large 741-bp 5′ untranslated region (UTR). H-NS represses transcription from PR3 at 20°C and binds both 5′ and 3′ of the transcription start site. The 3′ downstream regulatory element (DRE) was essential for temperature-dependent H-NS repression. At 37°C, SlyA activates transcription independent of H-NS but maximal transcription requires H-NS. The UTR is present between the transcription start site and the first gene in the operon, kpsM. We demonstrate that the UTR, as well as containing the H-NS DRE, functions to moderate the extent of transcription that reaches kpsM and allows the binding of antitermination factor RfaH.

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Mills, William T., Noor N. Nassar, Deepa Ravindra, Xinbei Li, and Mollie K. Meffert. "Multi-Level Regulatory Interactions between NF-κB and the Pluripotency Factor Lin28." Cells 9, no. 12 (December 17, 2020): 2710. http://dx.doi.org/10.3390/cells9122710.

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An appreciation for the complex interactions between the NF-κB transcription factor and the Lin28 RNA binding protein/let-7 microRNA pathways has grown substantially over the past decade. Both the NF-κB and Lin28/let-7 pathways are master regulators impacting cell survival, growth and proliferation, and an understanding of how interfaces between these pathways participate in governing pluripotency, progenitor differentiation, and neuroplastic responses remains an emerging area of research. In this review, we provide a concise summary of the respective pathways and focus on the function of signaling interactions at both the transcriptional and post-transcriptional levels. Regulatory loops capable of providing both reinforcing and extinguishing feedback have been described. We highlight convergent findings in disparate biological systems and indicate future directions for investigation.

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Qiu, Yichun, and Claudia Köhler. "Mobility connects: transposable elements wire new transcriptional networks by transferring transcription factor binding motifs." Biochemical Society Transactions 48, no. 3 (June 23, 2020): 1005–17. http://dx.doi.org/10.1042/bst20190937.

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Transposable elements (TEs) constitute major fractions of plant genomes. Their potential to be mobile provides them with the capacity to cause major genome rearrangements. Those effects are potentially deleterious and enforced the evolution of epigenetic suppressive mechanisms controlling TE activity. However, beyond their deleterious effects, TE insertions can be neutral or even advantageous for the host, leading to long-term retention of TEs in the host genome. Indeed, TEs are increasingly recognized as major drivers of evolutionary novelties by regulating the expression of nearby genes. TEs frequently contain binding motifs for transcription factors and capture binding motifs during transposition, which they spread through the genome by transposition. Thus, TEs drive the evolution and diversification of gene regulatory networks by recruiting lineage-specific targets under the regulatory control of specific transcription factors. This process can explain the rapid and repeated evolution of developmental novelties, such as C4 photosynthesis and a wide spectrum of stress responses in plants. It also underpins the convergent evolution of embryo nourishing tissues, the placenta in mammals and the endosperm in flowering plants. Furthermore, the gene regulatory network underlying flower development has also been largely reshaped by TE-mediated recruitment of regulatory elements; some of them being preserved across long evolutionary timescales. In this review, we highlight the potential role of TEs as evolutionary toolkits in plants by showcasing examples of TE-mediated evolutionary novelties.

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Hundley, Thomas R., Alasdair M. Gilfillan, Christine Tkaczyk, Marcus V. Andrade, Dean D. Metcalfe, and Michael A. Beaven. "Kit and FcϵRI mediate unique and convergent signals for release of inflammatory mediators from human mast cells." Blood 104, no. 8 (October 15, 2004): 2410–17. http://dx.doi.org/10.1182/blood-2004-02-0631.

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Abstract In human mast cells, derived from CD34+ peripheral blood cells, we observed that Kit ligand (KL) failed to induce degranulation but acted in synergy with antigen to markedly enhance degranulation, levels of cytokine gene transcripts, and production of cytokines. Further examination revealed that antigen and KL activated common and unique signaling pathways to account for these varied responses. KL, unlike antigen, failed to activate protein kinase C but activated phospholipase Cγ and calcium mobilization and augmented these signals as well as degranulation when added together with antigen. Both KL and antigen induced signals that are associated with cytokine production, namely phosphorylation of the mitogen-activated protein kinases, phosphatidylinositol 3–kinase–dependent phosphorylation of protein kinase B (also known as Akt), and phosphorylation of nuclear factor κB (NFκB). However, only KL stimulated phosphorylation of signal transducer and activator of transcription 5 (STAT5) and STAT6, whereas antigen weakly stimulated the protein kinase C–dependent induction and phosphorylation of c-Jun and associated activating protein-1 (AP-1) components, an action that was markedly potentiated by costimulation with KL. Interestingly, most signals were down-regulated on continuous exposure to KL but were reactivated along with cytokine gene transcription on addition of antigen. The findings, in total, indicated that a combination of FcϵRI and Kit-mediated signals and transcriptional processes were required for optimal physiologic responses of human mast cells to antigen.

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Crampton, Neal, William A. Bonass, Jennifer Kirkham, Claudio Rivetti, and Neil H. Thomson. "Collision events between RNA polymerases in convergent transcription studied by atomic force microscopy." Nucleic Acids Research 34, no. 19 (September 29, 2006): 5416–25. http://dx.doi.org/10.1093/nar/gkl668.

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Tsaneva-Atanasova, Krasimira, Christopher J. Caunt, Stephen P. Armstrong, Rebecca M. Perrett, and Craig A. McArdle. "Decoding neurohormone pulse frequency by convergent signalling modules." Biochemical Society Transactions 40, no. 1 (January 19, 2012): 273–78. http://dx.doi.org/10.1042/bst20110645.

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GnRH (gonadotropin-releasing hormone) mediates control of reproduction. It is secreted in pulses and acts via intracellular effectors to activate gene expression. Submaximal GnRH pulse frequency can elicit maximal responses, yielding bell-shaped frequency–response curves characteristic of genuine frequency decoders. GnRH frequency decoding is therapeutically important (pulsatile GnRH can drive ovulation in assisted reproduction, whereas sustained activation can treat breast and prostate cancers), but the mechanisms are unknown. In the present paper, we review recent work in this area, placing emphasis on the regulation of transcription, and showing how mathematical modelling of GnRH effects on two effectors [ERK (extracellular-signal-regulated kinase) and NFAT (nuclear factor of activated T-cells)] reveals the potential for genuine frequency decoding as an emergent feature of the GnRH signalling network, rather than an intrinsic feature of a given protein or pathway within it.

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Fang, Zhiming, Zhongming Zhao, Valsamma Eapen, and Raymond A. Clarke. "siRNA Mediate RNA Interference Concordant with Early On-Target Transient Transcriptional Interference." Genes 12, no. 8 (August 23, 2021): 1290. http://dx.doi.org/10.3390/genes12081290.

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Exogenous siRNAs are commonly used to regulate endogenous gene expression levels for gene function analysis, genotype–phenotype association studies and for gene therapy. Exogenous siRNAs can target mRNAs within the cytosol as well as nascent RNA transcripts within the nucleus, thus complicating siRNA targeting specificity. To highlight challenges in achieving siRNA target specificity, we targeted an overlapping gene set that we found associated with a familial form of multiple synostosis syndrome type 4 (SYSN4). In the affected family, we found that a previously unknown non-coding gene TOSPEAK/C8orf37AS1 was disrupted and the adjacent gene GDF6 was downregulated. Moreover, a conserved long-range enhancer for GDF6 was found located within TOSPEAK which in turn overlapped another gene which we named SMALLTALK/C8orf37. In fibroblast cell lines, SMALLTALK is transcribed at much higher levels in the opposite (convergent) direction to TOSPEAK. siRNA targeting of SMALLTALK resulted in post transcriptional gene silencing (PTGS/RNAi) of SMALLTALK that peaked at 72 h together with a rapid early increase in the level of both TOSPEAK and GDF6 that peaked and waned after 24 h. These findings indicated the following sequence of events: Firstly, the siRNA designed to target SMALLTALK mRNA for RNAi in the cytosol had also caused an early and transient transcriptional interference of SMALLTALK in the nucleus; Secondly, the resulting interference of SMALLTALK transcription increased the transcription of TOSPEAK; Thirdly, the increased transcription of TOSPEAK increased the transcription of GDF6. These findings have implications for the design and application of RNA and DNA targeting technologies including siRNA and CRISPR. For example, we used siRNA targeting of SMALLTALK to successfully restore GDF6 levels in the gene therapy of SYNS4 family fibroblasts in culture. To confidently apply gene targeting technologies, it is important to first determine the transcriptional interference effects of the targeting reagent and the targeted gene.

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Martínez-Calvillo, Santiago, Dan Nguyen, Kenneth Stuart, and Peter J. Myler. "Transcription Initiation and Termination on Leishmania major Chromosome 3." Eukaryotic Cell 3, no. 2 (April 2004): 506–17. http://dx.doi.org/10.1128/ec.3.2.506-517.2004.

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ABSTRACT Genome projects involving Leishmania and other trypanosomatids have revealed that most genes in these organisms are organized into large clusters of genes on the same DNA strand. We have previously shown that transcription of the entire Leishmania major Friedlin (LmjF) chromosome 1 (chr1) initiates bidirectionally between two divergent gene clusters. Here, we analyze transcription of LmjF chr3, which contains two convergent clusters of 67 and 30 genes, separated by a tRNA gene, with a single divergent protein-coding gene located close to the “left” telomere. Nuclear run-on analyses indicate that specific transcription of chr3 initiates bidirectionally between the single subtelomeric gene and the adjacent 67-gene cluster, close to the “right” telomere upstream of the 30-gene cluster, and upstream of the tRNA gene. Transcription on both strands terminates within the tRNA-gene region. Transient-transfection studies support the role of the tRNA-gene region as a transcription terminator for RNA polymerase II (Pol II) and Pol III, and also for Pol I.

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Jaeger, Tina, and Christoph Mayer. "The Transcriptional Factors MurR and Catabolite Activator Protein Regulate N-Acetylmuramic Acid Catabolism in Escherichia coli." Journal of Bacteriology 190, no. 20 (August 22, 2008): 6598–608. http://dx.doi.org/10.1128/jb.00642-08.

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ABSTRACT The MurNAc etherase MurQ of Escherichia coli is essential for the catabolism of the bacterial cell wall sugar N-acetylmuramic acid (MurNAc) obtained either from the environment or from the endogenous cell wall (i.e., recycling). High-level expression of murQ is required for growth on MurNAc as the sole source of carbon and energy, whereas constitutive low-level expression of murQ is sufficient for the recycling of peptidoglycan fragments continuously released from the cell wall during growth of the bacteria. Here we characterize for the first time the expression of murQ and its regulation by MurR, a member of the poorly characterized RpiR/AlsR family of transcriptional regulators. Deleting murR abolished the extensive lag phase observed for E. coli grown on MurNAc and enhanced murQ transcription some 20-fold. MurR forms a stable multimer (most likely a tetramer) and binds to two adjacent inverted repeats within an operator region. In this way MurR represses transcription from the murQ promoter and also interferes with its own transcription. MurNAc-6-phosphate, the substrate of MurQ, was identified as a specific inducer that weakens binding of MurR to the operator. Moreover, murQ transcription depends on the activation by cyclic AMP (cAMP)-catabolite activator protein (CAP) bound to a class I site upstream of the murQ promoter. murR and murQ are divergently orientated and expressed from nonoverlapping face-to-face (convergent) promoters, yielding transcripts that are complementary at their 5′ ends. As a consequence of this unusual promoter arrangement, cAMP-CAP also affects murR transcription, presumably by acting as a roadblock for RNA polymerase.

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Zhang, Xinyan, Meixia Zhao, Donald R. McCarty, and Damon Lisch. "Transposable elements employ distinct integration strategies with respect to transcriptional landscapes in eukaryotic genomes." Nucleic Acids Research 48, no. 12 (May 22, 2020): 6685–98. http://dx.doi.org/10.1093/nar/gkaa370.

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Abstract Transposable elements (TEs) are ubiquitous DNA segments capable of moving from one site to another within host genomes. The extant distributions of TEs in eukaryotic genomes have been shaped by both bona fide TE integration preferences in eukaryotic genomes and by selection following integration. Here, we compare TE target site distribution in host genomes using multiple de novo transposon insertion datasets in both plants and animals and compare them in the context of genome-wide transcriptional landscapes. We showcase two distinct types of transcription-associated TE targeting strategies that suggest a process of convergent evolution among eukaryotic TE families. The integration of two precision-targeting elements are specifically associated with initiation of RNA Polymerase II transcription of highly expressed genes, suggesting the existence of novel mechanisms of precision TE targeting in addition to passive targeting of open chromatin. We also highlight two features that can facilitate TE survival and rapid proliferation: tissue-specific transposition and minimization of negative impacts on nearby gene function due to precision targeting.

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Sameshima, J. H., R. C. Wek, and G. W. Hatfield. "Overlapping Transcription and Termination of the Convergent ilvA and ilvY Genes of Escherichia coli." Journal of Biological Chemistry 264, no. 2 (January 1989): 1224–31. http://dx.doi.org/10.1016/s0021-9258(19)85075-5.

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Chatterjee, Nimrat, Yunfu Lin, and John H. Wilson. "Mismatch repair enhances convergent transcription-induced cell death at trinucleotide repeats by activating ATR." DNA Repair 42 (June 2016): 26–32. http://dx.doi.org/10.1016/j.dnarep.2016.03.016.

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Chu, Jeffrey SC, David L. Baillie, and Nansheng Chen. "Convergent evolution of RFX transcription factors and ciliary genes predated the origin of metazoans." BMC Evolutionary Biology 10, no. 1 (2010): 130. http://dx.doi.org/10.1186/1471-2148-10-130.

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Tran, Ngat T., Michael T. Laub, and Tung B. K. Le. "SMC Progressively Aligns Chromosomal Arms in Caulobacter crescentus but Is Antagonized by Convergent Transcription." Cell Reports 20, no. 9 (August 2017): 2057–71. http://dx.doi.org/10.1016/j.celrep.2017.08.026.

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Chen, Kok-Siong, Jonathan W. C. Lim, Linda J. Richards, and Jens Bunt. "The convergent roles of the nuclear factor I transcription factors in development and cancer." Cancer Letters 410 (December 2017): 124–38. http://dx.doi.org/10.1016/j.canlet.2017.09.015.

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Blombach, Fabian, Tina Daviter, Daniel Fielden, Dina Grohmann, Katherine Smollett, and Finn Werner. "Archaeology of RNA polymerase: factor swapping during the transcription cycle." Biochemical Society Transactions 41, no. 1 (January 29, 2013): 362–67. http://dx.doi.org/10.1042/bst20120274.

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All RNAPs (RNA polymerases) repeatedly make use of their DNA template by progressing through the transcription cycle multiple times. During transcription initiation and elongation, distinct sets of transcription factors associate with multisubunit RNAPs and modulate their nucleic-acid-binding and catalytic properties. Between the initiation and elongation phases of the cycle, the factors have to be exchanged by a largely unknown mechanism. We have shown that the binding sites for initiation and elongation factors are overlapping and that the binding of the factors to RNAP is mutually exclusive. This ensures an efficient exchange or ‘swapping’ of factors and could furthermore assist RNAP during promoter escape, enabling robust transcription. A similar mechanism applies to the bacterial RNAP system. The elongation factors are evolutionarily conserved between the bacterial (NusG) and archaeo-eukaryotic (Spt5) systems; however, the initiation factors [σ and TBP (TATA-box-binding protein)/TF (transcription factor) B respectively] are not. Therefore we propose that this factor-swapping mechanism, operating in all three domains of life, is the outcome of convergent evolution.

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O’Donovan, Aoife, Bing Sun, Steve Cole, Hans Rempel, Maryann Lenoci, Lynn Pulliam, and Thomas Neylan. "Transcriptional Control of Monocyte Gene Expression in Post-Traumatic Stress Disorder." Disease Markers 30, no. 2-3 (2011): 123–32. http://dx.doi.org/10.1155/2011/560572.

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Post-traumatic stress disorder (PTSD) confers an increased risk for disorders with an inflammatory etiology. PTSD-related dysregulation of the sympathetic nervous system (SNS) and hypothalamic-pituitary adrenal (HPA) axis and associated alterations in inflammatory activity may contribute to this increased risk. However, little is known about convergent SNS, HPA and inflammatory signaling at the level of the immune cell transcriptome in PTSD. To explore such signaling, we examined the prevalence of specific transcription factor binding motifs in the promoter regions of differentially expressed genes in monocytes from individuals with PTSD and matched controls. Participants included 49 men (24 PTSD+ and 25 trauma-exposed controls) and 18 women (10 PTSD+ and 8 controls). Men with PTSD showed up-regulation of target genes for the NF-κB/Rel family of transcription factors, which convey inflammatory signals, up-regulation of target genes for CREB/ATF transcription factors, which convey adrenergic signals from the SNS, and down-regulation of target genes for the glucocorticoid receptor, which conveys glucocorticoid signals from the HPA axis. Women with PTSD also showed significant up-regulation of target genes for NF-κB and non-significant down-regulation of target genes for GR, but significant down-regulation of target genes for CREB/ATF. Altered transcriptional control of monocyte gene expression could contribute to exaggerated inflammatory activity in PTSD.

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García-Rubio, María L., and Andrés Aguilera. "Topological constraints impair RNA polymerase II transcription and causes instability of plasmid-borne convergent genes." Nucleic Acids Research 40, no. 3 (October 13, 2011): 1050–64. http://dx.doi.org/10.1093/nar/gkr840.

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Deeble, Paul D., Daniel J. Murphy, Sarah J. Parsons, and Michael E. Cox. "Interleukin-6- and Cyclic AMP-Mediated Signaling Potentiates Neuroendocrine Differentiation of LNCaP Prostate Tumor Cells." Molecular and Cellular Biology 21, no. 24 (December 15, 2001): 8471–82. http://dx.doi.org/10.1128/mcb.21.24.8471-8482.2001.

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ABSTRACT Neuroendocrine (NE) differentiation in prostatic adenocarcinomas has been reported to be an early marker for development of androgen independence. Secretion of mitogenic peptides from nondividing NE cells is thought to contribute to a more aggressive disease by promoting the proliferation of surrounding tumor cells. We undertook studies to determine whether the prostate cancer cell line LNCaP could be induced to acquire NE characteristics by treatment with agents that are found in the complex environment in which progression of prostate cancer towards androgen independence occurs. We found that cotreatment of LNCaP cells with agents that signal through cyclic AMP-dependent protein kinase (PKA), such as epinephrine and forskolin, and with the cytokine interleukin-6 (IL-6) promoted the acquisition of an NE morphological phenotype above that seen with single agents. Convergent IL-6 and PKA signaling also resulted in potentiated mitogen-activated protein kinase (MAPK) activation without affecting the level of signal transducer and activator of transcription or PKA activation observed with these agents alone. Cotreatment with epinephrine and IL-6 synergistically increased c-fos transcription as well as transcription from the β4 nicotinic acetylcholine receptor subunit promoter. Potentiated transcription from these elements was shown to be dependent on the MAPK pathway. Most importantly, cotreatment with PKA activators and IL-6 resulted in increased secretion of mitogenic neuropeptides. These results indicate that PKA and IL-6 signaling participates in gene transcriptional changes that reflect acquisition of an NE phenotype by LNCaP cells and suggest that similar signaling mechanisms, particularly at sites of metastasis, may be responsible for the increased NE content of many advanced prostate carcinomas.

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Arnone, James T., Jeffrey R. Arace, Anand R. Soorneedi, Teryn T. Citino, Tadashi L. Kamitaki, and Michael A. McAlear. "Dissecting thecisandtransElements That Regulate Adjacent-Gene Coregulation in Saccharomyces cerevisiae." Eukaryotic Cell 13, no. 6 (April 4, 2014): 738–48. http://dx.doi.org/10.1128/ec.00317-13.

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ABSTRACTThe relative positions that genes occupy on their respective chromosomes can play a critical role in determining how they are regulated at the transcriptional level. For example, a significant fraction of the genes from a variety of coregulated gene sets, including the ribosomal protein (RP) and the rRNA and ribosome biogenesis (RRB) regulons, exist as immediate, adjacent gene pairs. These gene pairs occur in all possible divergent, tandem, and convergent orientations. Adjacent-gene pairing in these regulons is associated with a tighter transcriptional coregulation than is observed for nonpaired genes of the same regulons. In order to define thecisandtransfactors that regulate adjacent-gene coregulation (AGC), we conducted a mutational analysis of the convergently oriented RRB gene pairMPP10-YJR003C. We observed that coupled corepression of the gene pair under heat shock was abrogated when the two genes were separated by an actively expressed RNA polymerase (Pol) II transcription unit (theLEU2gene) but not when the insertedLEU2gene was repressed. In contrast, the insertion of an RNA Pol III-transcribed tRNA (Thr) gene did not disrupt the coregulated repression ofMPP10andYJR003C. A targeted screen of mutants defective in regulating chromosome architecture revealed that the Spt20, Snf2, and Chd1 proteins were required for coupling the repression ofYJR003Cto that ofMPP10. Nucleosome occupancy assays performed across theMPP10andYJR003Cpromoter regions revealed that the mechanism of corepression of the gene pair was not related to the repositioning of nucleosomes across the respective gene promoters.

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Georgieva, L., V. Moskvina, T. Peirce, N. Norton, N. J. Bray, L. Jones, P. Holmans, et al. "Convergent evidence that oligodendrocyte lineage transcription factor 2 (OLIG2) and interacting genes influence susceptibility to schizophrenia." Proceedings of the National Academy of Sciences 103, no. 33 (August 4, 2006): 12469–74. http://dx.doi.org/10.1073/pnas.0603029103.

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Schmitt, Rebecca E., Brandon C. Shell, Kristen M. Lee, Keith L. Shelton, Laura D. Mathies, Alexis C. Edwards, and Mike Grotewiel. "Convergent Evidence From Humans and Drosophila melanogaster Implicates the Transcription Factor MEF2B / Mef2 in Alcohol Sensitivity." Alcoholism: Clinical and Experimental Research 43, no. 9 (July 16, 2019): 1872–86. http://dx.doi.org/10.1111/acer.14138.

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Liu, Zheng, Shuangcheng Gao, Shumin Zhang, Shangjun Yang, and Ning Sun. "Complex structures of transgene rearrangement implicate novel mechanisms of RNA-directed DNA methylation and convergent transcription." Genes & Genomics 36, no. 1 (September 26, 2013): 95–103. http://dx.doi.org/10.1007/s13258-013-0147-8.

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Wilinski, Daniel, Natascha Buter, Andrew D. Klocko, Christopher P. Lapointe, Eric U. Selker, Audrey P. Gasch, and Marvin Wickens. "Recurrent rewiring and emergence of RNA regulatory networks." Proceedings of the National Academy of Sciences 114, no. 14 (March 20, 2017): E2816—E2825. http://dx.doi.org/10.1073/pnas.1617777114.

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Alterations in regulatory networks contribute to evolutionary change. Transcriptional networks are reconfigured by changes in the binding specificity of transcription factors and their cognate sites. The evolution of RNA–protein regulatory networks is far less understood. The PUF (Pumilio and FBF) family of RNA regulatory proteins controls the translation, stability, and movements of hundreds of mRNAs in a single species. We probe the evolution of PUF–RNA networks by direct identification of the mRNAs bound to PUF proteins in budding and filamentous fungi and by computational analyses of orthologous RNAs from 62 fungal species. Our findings reveal that PUF proteins gain and lose mRNAs with related and emergent biological functions during evolution. We demonstrate at least two independent rewiring events for PUF3 orthologs, independent but convergent evolution of PUF4/5 binding specificity and the rewiring of the PUF4/5 regulons in different fungal lineages. These findings demonstrate plasticity in RNA regulatory networks and suggest ways in which their rewiring occurs.

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Howell, Michael, Gareth J. Inman, and Caroline S. Hill. "A novel Xenopus Smad-interacting forkhead transcription factor (XFast-3) cooperates with XFast-1 in regulating gastrulation movements." Development 129, no. 12 (June 15, 2002): 2823–34. http://dx.doi.org/10.1242/dev.129.12.2823.

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In early Xenopus embryos, the prototypical XFast-1/Smad2/Smad4 complex ARF1 is induced at the Mix.2 ARE by activin overexpression. We have characterised ARF2, a related, but much more abundant, complex formed during gastrulation in response to endogenous TGFβ family members and we have identified a novel Fast family member, XFast-3, as its transcription factor component. Endogenous ARF2 efficiently competes out ARF1 at early gastrulation, due to the ability of XFast-3 to interact with activated Smads with much higher affinity than XFast-1. We demonstrate that ARF1 and ARF2 are activated by distinct TGFβ family members. Using morpholino antisense oligonucleotides to deplete levels of the constituent transcription factors XFast-1 and XFast-3 specifically, we demonstrate an important role for ARF1 and ARF2 in early Xenopus embryos in controlling the convergent extension movements of gastrulation.

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Pénzes, Judit J., Hanh T. Pham, Paul Chipman, Nilakshee Bhattacharya, Robert McKenna, Mavis Agbandje-McKenna, and Peter Tijssen. "Molecular biology and structure of a novel penaeid shrimp densovirus elucidate convergent parvoviral host capsid evolution." Proceedings of the National Academy of Sciences 117, no. 33 (August 3, 2020): 20211–22. http://dx.doi.org/10.1073/pnas.2008191117.

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The giant tiger prawn (Penaeus monodon) is a decapod crustacean widely reared for human consumption. Currently, viruses of two distinct lineages of parvoviruses (PVs, familyParvoviridae; subfamilyHamaparvovirinae) infect penaeid shrimp. Here, a PV was isolated and cloned from VietnameseP. monodonspecimens, designatedPenaeus monodonmetallodensovirus (PmMDV). This is the first member of a third divergent lineage shown to infect penaeid decapods. PmMDV has a transcription strategy unique among invertebrate PVs, using extensive alternative splicing and incorporating transcription elements characteristic of vertebrate-infecting PVs. The PmMDV proteins have no significant sequence similarity with other PVs, except for an SF3 helicase domain in its nonstructural protein. Its capsid structure, determined by cryoelectron microscopy to 3-Å resolution, has a similar surface morphology toPenaeus stylirostrisdensovirus, despite the lack of significant capsid viral protein (VP) sequence similarity. Unlike other PVs, PmMDV folds its VP without incorporating a βA strand and displayed unique multimer interactions, including the incorporation of a Ca2+cation, attaching the N termini under the icosahedral fivefold symmetry axis, and forming a basket-like pentamer helix bundle. While the PmMDV VP sequence lacks a canonical phospholipase A2 domain, the structure of an EDTA-treated capsid, determined to 2.8-Å resolution, suggests an alternative membrane-penetrating cation-dependent mechanism in its N-terminal region. PmMDV is an observed example of convergent evolution among invertebrate PVs with respect to host-driven capsid structure and unique as a PV showing a cation-sensitive/dependent basket structure for an alternative endosomal egress.

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Minchiotti, G., and P. P. Di Nocera. "Convergent transcription initiates from oppositely oriented promoters within the 5' end regions of Drosophila melanogaster F elements." Molecular and Cellular Biology 11, no. 10 (October 1991): 5171–80. http://dx.doi.org/10.1128/mcb.11.10.5171-5180.1991.

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Drosophila melanogaster F elements are mobile, oligo(A)-terminated DNA sequences that likely propagate by the retrotranscription of RNA intermediates. Plasmids bearing DNA segments from the left-hand region of a full-length F element fused to the CAT gene were used as templates for transient expression assays in Drosophila Schneider II cultured cells. Protein and RNA analyses led to the identification of two promoters, Fin and Fout, that transcribe in opposite orientations. The Fin promoter drives the synthesis of transcripts that initiate around residue +6 and are directed toward the element. Fin, that probably controls the formation of F transposition RNA intermediates and gene products, is internal to the transcribed region. Sequences important for accumulation of Fin transcripts are included within the +1 to +30 interval; an additional regulatory element may coincide with a heptamer located downstream of this region also found in the 5' end regions of F-like Drosophila retrotransposons. Analysis of the template activity of 3' deletion derivatives indicates that the level of accumulation of Fin RNA is also dependent upon the presence of sequences located within the +175 to +218 interval. The Fout promoter drives transcription in the opposite orientation with respect to Fin. Fout transcripts initiate at nearby sites within the +92 to +102 interval. Sequences downstream of these multiple RNA start sites are not required for the activity of the Fout promoter. Deletions knocking out the Fin promoter do not impair Fout transcription; conversely, initiation at the Fin promoter still takes place in templates that lack the Fout promoter. At a low level, both promoters are active in cultured cells.

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Minchiotti, G., and P. P. Di Nocera. "Convergent transcription initiates from oppositely oriented promoters within the 5' end regions of Drosophila melanogaster F elements." Molecular and Cellular Biology 11, no. 10 (October 1991): 5171–80. http://dx.doi.org/10.1128/mcb.11.10.5171.

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Drosophila melanogaster F elements are mobile, oligo(A)-terminated DNA sequences that likely propagate by the retrotranscription of RNA intermediates. Plasmids bearing DNA segments from the left-hand region of a full-length F element fused to the CAT gene were used as templates for transient expression assays in Drosophila Schneider II cultured cells. Protein and RNA analyses led to the identification of two promoters, Fin and Fout, that transcribe in opposite orientations. The Fin promoter drives the synthesis of transcripts that initiate around residue +6 and are directed toward the element. Fin, that probably controls the formation of F transposition RNA intermediates and gene products, is internal to the transcribed region. Sequences important for accumulation of Fin transcripts are included within the +1 to +30 interval; an additional regulatory element may coincide with a heptamer located downstream of this region also found in the 5' end regions of F-like Drosophila retrotransposons. Analysis of the template activity of 3' deletion derivatives indicates that the level of accumulation of Fin RNA is also dependent upon the presence of sequences located within the +175 to +218 interval. The Fout promoter drives transcription in the opposite orientation with respect to Fin. Fout transcripts initiate at nearby sites within the +92 to +102 interval. Sequences downstream of these multiple RNA start sites are not required for the activity of the Fout promoter. Deletions knocking out the Fin promoter do not impair Fout transcription; conversely, initiation at the Fin promoter still takes place in templates that lack the Fout promoter. At a low level, both promoters are active in cultured cells.

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Chatterjee, Anushree, Laurie Drews, Sarika Mehra, Eriko Takano, Yiannis N. Kaznessis, and Wei-Shou Hu. "Convergent Transcription in the Butyrolactone Regulon in Streptomyces coelicolor Confers a Bistable Genetic Switch for Antibiotic Biosynthesis." PLoS ONE 6, no. 7 (July 12, 2011): e21974. http://dx.doi.org/10.1371/journal.pone.0021974.

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Journal articles on the topic 'Convergent transcription'

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