Journal articles: 'Transcription Start Sites'

1

Stamatoyannopoulos, John A. "Illuminating eukaryotic transcription start sites." Nature Methods 7, no. 7 (July 2010): 501–3. http://dx.doi.org/10.1038/nmeth0710-501.

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2

Nielsen, Mathias, Ryan Ard, Xueyuan Leng, Maxim Ivanov, Peter Kindgren, Vicent Pelechano, and Sebastian Marquardt. "Transcription-driven chromatin repression of Intragenic transcription start sites." PLOS Genetics 15, no. 2 (February 1, 2019): e1007969. http://dx.doi.org/10.1371/journal.pgen.1007969.

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3

Li, W. Z., and F. Sherman. "Two types of TATA elements for the CYC1 gene of the yeast Saccharomyces cerevisiae." Molecular and Cellular Biology 11, no. 2 (February 1991): 666–76. http://dx.doi.org/10.1128/mcb.11.2.666-676.1991.

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Functional TATA elements in the 5' untranslated region of the CYC1 gene in the yeast Saccharomyces cerevisiae have been defined by transcriptional analysis of site-directed mutations. Five sites previously suggested to contain functional TATA elements were altered individually and in all possible combinations. The results indicated that only two elements are required for transcription at the normal level and the normal start sites. The two functional TATA elements are located at sites -178 and -123, where the A of the ATG start codon is assigned nucleotide position +1. They direct initiation within windows encompassing -70 to -46 and -46 to -28, respectively. Only when both of the upstream TATA sites were rendered nonfunctional were the third and fourth downstream TATA-like sequences activated, as indicated by the presence of low levels of transcription starting at -28. The two upstream functional TATA elements differed in sequence. The sequence of the most 5' one at site 1, denoted beta-type, was ATATATATAT, whereas that of the second one at site 2, denoted alpha-type, was TATATAAAA. The following rearrangements of the beta-type and alpha-type elements at two sites (1 and 2) were examined: site1 beta-site2 alpha; site 1 alpha-site 2 beta; site1 alpha-site2 alpha; and site1 beta-site2 beta. When different types were at different sites (site1 beta-site2 alpha and site1 alpha-site2 beta), both were used equally. In contrast, when the same type was present at both sites (site1 alpha-site2 alpha and site1 beta-site2 beta), only the upstream element was used. We suggest that the two TATA elements are recognized by different factors of the transcription apparatus.

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4

Li, W. Z., and F. Sherman. "Two types of TATA elements for the CYC1 gene of the yeast Saccharomyces cerevisiae." Molecular and Cellular Biology 11, no. 2 (February 1991): 666–76. http://dx.doi.org/10.1128/mcb.11.2.666.

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Functional TATA elements in the 5' untranslated region of the CYC1 gene in the yeast Saccharomyces cerevisiae have been defined by transcriptional analysis of site-directed mutations. Five sites previously suggested to contain functional TATA elements were altered individually and in all possible combinations. The results indicated that only two elements are required for transcription at the normal level and the normal start sites. The two functional TATA elements are located at sites -178 and -123, where the A of the ATG start codon is assigned nucleotide position +1. They direct initiation within windows encompassing -70 to -46 and -46 to -28, respectively. Only when both of the upstream TATA sites were rendered nonfunctional were the third and fourth downstream TATA-like sequences activated, as indicated by the presence of low levels of transcription starting at -28. The two upstream functional TATA elements differed in sequence. The sequence of the most 5' one at site 1, denoted beta-type, was ATATATATAT, whereas that of the second one at site 2, denoted alpha-type, was TATATAAAA. The following rearrangements of the beta-type and alpha-type elements at two sites (1 and 2) were examined: site1 beta-site2 alpha; site 1 alpha-site 2 beta; site1 alpha-site2 alpha; and site1 beta-site2 beta. When different types were at different sites (site1 beta-site2 alpha and site1 alpha-site2 beta), both were used equally. In contrast, when the same type was present at both sites (site1 alpha-site2 alpha and site1 beta-site2 beta), only the upstream element was used. We suggest that the two TATA elements are recognized by different factors of the transcription apparatus.

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5

Frith, M. C. "Evolutionary turnover of mammalian transcription start sites." Genome Research 16, no. 6 (June 1, 2006): 713–22. http://dx.doi.org/10.1101/gr.5031006.

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6

Gordon, J. J., M. W. Towsey, J. M. Hogan, S. A. Mathews, and P. Timms. "Improved prediction of bacterial transcription start sites." Bioinformatics 22, no. 2 (November 15, 2005): 142–48. http://dx.doi.org/10.1093/bioinformatics/bti771.

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7

Drysdale, Melissa, Agathe Bourgogne, and Theresa M. Koehler. "Transcriptional Analysis of the Bacillus anthracis Capsule Regulators." Journal of Bacteriology 187, no. 15 (August 1, 2005): 5108–14. http://dx.doi.org/10.1128/jb.187.15.5108-5114.2005.

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ABSTRACT The poly-d-glutamic acid capsule of Bacillus anthracis is essential for virulence. Control of capsule synthesis occurs at the level of transcription and involves positive regulation of the capsule biosynthetic operon capBCAD by a CO2/bicarbonate signal and three plasmid-borne regulators: atxA, acpA, and acpB. Although the molecular mechanism for control of cap transcription is unknown, atxA affects cap expression via positive control of acpA and acpB, two genes with partial functional similarity. Transcriptional analyses of a genetically complete strain indicate that capB expression is several hundred-fold higher during growth in 5% CO2 compared to growth in air. atxA was expressed appreciably during growth in air and induced only 2.5-fold by CO2. In contrast, expression of acpA and acpB was induced up to 23-fold and 59-fold, respectively, by CO2. The 5′-end mapping of gene transcripts revealed atxA-regulated and atxA-independent apparent transcription start sites for capB, acpA, and acpB. Transcripts mapping to all atxA-regulated start sites were increased during growth in elevated CO2. The acpA gene has one atxA-regulated and one atxA-independent start site. acpB lies downstream of capBCAD. A single atxA-independent start site maps immediately upstream of acpB. atxA-mediated control of acpB appears to occur via transcriptional read-through from atxA-dependent start sites 5′ of capB. One atxA-independent and two atxA-regulated start sites map upstream of capB. Transcription from the atxA-regulated start sites of capBCAD was reduced significantly in an acpA acpB double mutant but unaffected in mutants with deletion of only acpA or acpB, in agreement with the current model for epistatic relationships between the regulators.

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8

Membrillo-Hernández, Jorge, and E. C. C. Lin. "Regulation of Expression of the adhE Gene, Encoding Ethanol Oxidoreductase in Escherichia coli: Transcription from a Downstream Promoter and Regulation by Fnr and RpoS." Journal of Bacteriology 181, no. 24 (December 15, 1999): 7571–79. http://dx.doi.org/10.1128/jb.181.24.7571-7579.1999.

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ABSTRACT The adhE gene of Escherichia coli, located at min 27 on the chromosome, encodes the bifunctional NAD-linked oxidoreductase responsible for the conversion of acetyl-coenzyme A to ethanol during fermentative growth. The expression of adhEis dependent on both transcriptional and posttranscriptional controls and is about 10-fold higher during anaerobic than during aerobic growth. Two putative transcriptional start sites have been reported: one at position −292 and the other at −188 from the translational start codon ATG. In this study we show, by using several different transcriptional and translational fusions to the lacZ gene, that both putative transcriptional start sites can be functional and each site can be redox regulated. Although both start sites are NarL repressible in the presence of nitrate, Fnr activates only the −188 start site and Fis is required for the transcription of only the −292 start site. In addition, it was discovered that RpoS activatesadhE transcription at both start sites. Under all experimental conditions tested, however, only the upstream start site is active. Available evidence indicates that under those conditions, the upstream promoter region acts as a silencer of the downstream transcriptional start site. Translation of the mRNA starting at −292, but not the one starting at −188, requires RNase III. The results support the previously postulated ribosomal binding site (RBS) occlusion model, according to which RNase III cleavage is required to release the RBS from a stem-loop structure in the long transcript.

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9

Howcroft, T. Kevin, Aparna Raval, Jocelyn D. Weissman, Anne Gegonne, and Dinah S. Singer. "Distinct Transcriptional Pathways Regulate Basal and Activated Major Histocompatibility Complex Class I Expression." Molecular and Cellular Biology 23, no. 10 (May 15, 2003): 3377–91. http://dx.doi.org/10.1128/mcb.23.10.3377-3391.2003.

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ABSTRACT Transcription of major histocompatibility complex (MHC) class I genes is regulated by both tissue-specific (basal) and hormone/cytokine (activated) mechanisms. Although promoter-proximal regulatory elements have been characterized extensively, the role of the core promoter in mediating regulation has been largely undefined. We report here that the class I core promoter consists of distinct elements that are differentially utilized in basal and activated transcription pathways. These pathways recruit distinct transcription factor complexes to the core promoter elements and target distinct transcription initiation sites. Class I transcription initiates at four major sites within the core promoter and is clustered in two distinct regions: “upstream” (−14 and −18) and “downstream” (+12 and +1). Basal transcription initiates predominantly from the upstream start site region and is completely dependent upon the general transcription factor TAF1 (TAFII250). Activated transcription initiates predominantly from the downstream region and is TAF1 (TAFII250) independent. USF1 augments transcription initiating through the upstream start sites and is dependent on TAF1 (TAFII250), a finding consistent with its role in regulating basal class I transcription. In contrast, transcription activated by the interferon mediator CIITA is independent of TAF1 (TAFII250) and focuses initiation on the downstream start sites. Thus, basal and activated transcriptions of an MHC class I gene target distinct core promoter domains, nucleate distinct transcription initiation complexes and initiate at distinct sites within the promoter. We propose that transcription initiation at the core promoter is a dynamic process in which the mechanisms of core promoter function differ depending on the cellular environment.

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10

Ishihara, Satoru, Yohei Sasagawa, Takeru Kameda, Hayato Yamashita, Mana Umeda, Naoe Kotomura, Masayuki Abe, Yohei Shimono, and Itoshi Nikaido. "Local states of chromatin compaction at transcription start sites control transcription levels." Nucleic Acids Research 49, no. 14 (July 7, 2021): 8007–23. http://dx.doi.org/10.1093/nar/gkab587.

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Abstract The ‘open’ and ‘compact’ regions of chromatin are considered to be regions of active and silent transcription, respectively. However, individual genes produce transcripts at different levels, suggesting that transcription output does not depend on the simple open-compact conversion of chromatin, but on structural variations in chromatin itself, which so far have remained elusive. In this study, weakly crosslinked chromatin was subjected to sedimentation velocity centrifugation, which fractionated the chromatin according to its degree of compaction. Open chromatin remained in upper fractions, while compact chromatin sedimented to lower fractions depending on the level of nucleosome assembly. Although nucleosomes were evenly detected in all fractions, histone H1 was more highly enriched in the lower fractions. H1 was found to self-associate and crosslinked to histone H3, suggesting that H1 bound to H3 interacts with another H1 in an adjacent nucleosome to form compact chromatin. Genome-wide analyses revealed that nearly the entire genome consists of compact chromatin without differences in compaction between repeat and non-repeat sequences; however, active transcription start sites (TSSs) were rarely found in compact chromatin. Considering the inverse correlation between chromatin compaction and RNA polymerase binding at TSSs, it appears that local states of chromatin compaction determine transcription levels.

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11

Mendoza-Vargas, Alfredo, Leticia Olvera, Maricela Olvera, Ricardo Grande, Leticia Vega-Alvarado, Blanca Taboada, Verónica Jimenez-Jacinto, et al. "Genome-Wide Identification of Transcription Start Sites, Promoters and Transcription Factor Binding Sites in E. coli." PLoS ONE 4, no. 10 (October 19, 2009): e7526. http://dx.doi.org/10.1371/journal.pone.0007526.

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12

Holwerda, Sjoerd Johannes Bastiaan, and Wouter de Laat. "CTCF: the protein, the binding partners, the binding sites and their chromatin loops." Philosophical Transactions of the Royal Society B: Biological Sciences 368, no. 1620 (June 19, 2013): 20120369. http://dx.doi.org/10.1098/rstb.2012.0369.

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CTCF has it all. The transcription factor binds to tens of thousands of genomic sites, some tissue-specific, others ultra-conserved. It can act as a transcriptional activator, repressor and insulator, and it can pause transcription. CTCF binds at chromatin domain boundaries, at enhancers and gene promoters, and inside gene bodies. It can attract many other transcription factors to chromatin, including tissue-specific transcriptional activators, repressors, cohesin and RNA polymerase II, and it forms chromatin loops. Yet, or perhaps therefore, CTCF's exact function at a given genomic site is unpredictable. It appears to be determined by the associated transcription factors, by the location of the binding site relative to the transcriptional start site of a gene, and by the site's engagement in chromatin loops with other CTCF-binding sites, enhancers or gene promoters. Here, we will discuss genome-wide features of CTCF binding events, as well as locus-specific functions of this remarkable transcription factor.

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13

Kaebernick, Melanie, Elke Dittmann, Thomas BÃ¯Â¿Â½rner, and Brett A. Neilan. "Multiple Alternate Transcripts Direct the Biosynthesis of Microcystin, a Cyanobacterial." Applied and Environmental Microbiology 68, no. 2 (February 2002): 449–55. http://dx.doi.org/10.1128/aem.68.2.449-455.2002.

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ABSTRACT The mcyABCDEFGHIJ gene cluster of Microcystis aeruginosa encodes the mixed polyketide synthase/nonribosomal peptide synthetase (microcystin synthetase) which is responsible for biosynthesis of the potent liver toxin microcystin. The sequence and orientation of the mcy genes have previously been reported, but no transcriptional analysis had been performed prior to this study. The mcyABCDEFGHIJ genes are transcribed as two polycistronic operons, mcyABC and mcyDEFGHIJ, from a central bidirectional promoter between mcyA and mcyD. Two transcription start sites were detected for both mcyA and mcyD when cells were exposed to light intensities of 68 and 16 μmol of photons m−2 s−1. The start sites, located 206 and 254 bp upstream of the translational start for mcyD under high and low light conditions, respectively, indicate long untranslated leader regions. Putative transcription start sites were also identified for mcyE, mcyF, mcyG, mcyH, mcyI, and mcyJ but not for mcyB and mcyC. A combination of reverse transcription-PCR and rapid amplification of cDNA ends was employed throughout this work, which may have been one of the first transcriptional analyses of a large nonribosomal polyketide gene cluster.

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Bondar, Eugeniya I., Maxim E. Troukhan, Konstantin V. Krutovsky, and Tatiana V. Tatarinova. "Genome-Wide Prediction of Transcription Start Sites in Conifers." International Journal of Molecular Sciences 23, no. 3 (February 3, 2022): 1735. http://dx.doi.org/10.3390/ijms23031735.

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The identification of promoters is an essential step in the genome annotation process, providing a framework for gene regulatory networks and their role in transcription regulation. Despite considerable advances in the high-throughput determination of transcription start sites (TSSs) and transcription factor binding sites (TFBSs), experimental methods are still time-consuming and expensive. Instead, several computational approaches have been developed to provide fast and reliable means for predicting the location of TSSs and regulatory motifs on a genome-wide scale. Numerous studies have been carried out on the regulatory elements of mammalian genomes, but plant promoters, especially in gymnosperms, have been left out of the limelight and, therefore, have been poorly investigated. The aim of this study was to enhance and expand the existing genome annotations using computational approaches for genome-wide prediction of TSSs in the four conifer species: loblolly pine, white spruce, Norway spruce, and Siberian larch. Our pipeline will be useful for TSS predictions in other genomes, especially for draft assemblies, where reliable TSS predictions are not usually available. We also explored some of the features of the nucleotide composition of the predicted promoters and compared the GC properties of conifer genes with model monocot and dicot plants. Here, we demonstrate that even incomplete genome assemblies and partial annotations can be a reliable starting point for TSS annotation. The results of the TSS prediction in four conifer species have been deposited in the Persephone genome browser, which allows smooth visualization and is optimized for large data sets. This work provides the initial basis for future experimental validation and the study of the regulatory regions to understand gene regulation in gymnosperms.

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15

Lizio, Marina, Ruslan Deviatiiarov, Hiroki Nagai, Laura Galan, Erik Arner, Masayoshi Itoh, Timo Lassmann, et al. "Systematic analysis of transcription start sites in avian development." PLOS Biology 15, no. 9 (September 5, 2017): e2002887. http://dx.doi.org/10.1371/journal.pbio.2002887.

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16

Wakaguri, H., R. Yamashita, Y. Suzuki, S. Sugano, and K. Nakai. "DBTSS: database of transcription start sites, progress report 2008." Nucleic Acids Research 36, Database (December 23, 2007): D97—D101. http://dx.doi.org/10.1093/nar/gkm901.

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17

Reddy, D. Ashok, and Chanchal K. Mitra. "Comparative Analysis of Transcription Start Sites Using Mutual Information." Genomics, Proteomics & Bioinformatics 4, no. 3 (2006): 189–95. http://dx.doi.org/10.1016/s1672-0229(06)60032-6.

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Pavé-Preux, M., M. Aggerbeck, C. Veyssier, B. Bousquet-Lemercier, J. Hanoune, and R. Barouki. "Hormonal discrimination among transcription start sites of aspartate aminotransferase." Journal of Biological Chemistry 265, no. 8 (March 1990): 4444–48. http://dx.doi.org/10.1016/s0021-9258(19)39584-5.

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TOWSEY, MICHAEL W., JAMES J. GORDON, and JAMES M. HOGAN. "THE PREDICTION OF BACTERIAL TRANSCRIPTION START SITES USING SVMS." International Journal of Neural Systems 16, no. 05 (October 2006): 363–70. http://dx.doi.org/10.1142/s0129065706000767.

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Identifying promoters is the key to understanding gene expression in bacteria. Promoters lie in tightly constrained positions relative to the transcription start site (TSS). In this paper, we address the problem of predicting transcription start sites in Escherichia coli. Knowing the TSS position, one can then predict the promoter position to within a few base pairs, and vice versa. The accepted method for promoter prediction is to use a pair of position weight matrices (PWMs), which define conserved motifs at the sigma-factor binding site. However this method is known to result in a large number of false positive predictions, thereby limiting its usefulness to the experimental biologist. We adopt an alternative approach based on the Support Vector Machine (SVM) using a modified mismatch spectrum kernel. Our modifications involve tagging the motifs with their location, and selectively pruning the feature set. We quantify the performance of several SVM models and a PWM model using a performance metric of area under the detection-error tradeoff (DET) curve. SVM models are shown to outperform the PWM on a biologically realistic TSS prediction task. We also describe a more broadly applicable peak scoring technique which reduces the number of false positive predictions, greatly enhancing the utility of our results.

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20

Taft, Ryan J., Evgeny A. Glazov, Nicole Cloonan, Cas Simons, Stuart Stephen, Geoffrey J. Faulkner, Timo Lassmann, et al. "Tiny RNAs associated with transcription start sites in animals." Nature Genetics 41, no. 5 (April 19, 2009): 572–78. http://dx.doi.org/10.1038/ng.312.

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21

Fu, Ye, Guan-Zheng Luo, Kai Chen, Xin Deng, Miao Yu, Dali Han, Ziyang Hao, et al. "N6-Methyldeoxyadenosine Marks Active Transcription Start Sites in Chlamydomonas." Cell 161, no. 4 (May 2015): 879–92. http://dx.doi.org/10.1016/j.cell.2015.04.010.

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22

Chang, D. D., and D. A. Clayton. "Precise assignment of the heavy-strand promoter of mouse mitochondrial DNA: cognate start sites are not required for transcriptional initiation." Molecular and Cellular Biology 6, no. 9 (September 1986): 3262–67. http://dx.doi.org/10.1128/mcb.6.9.3262-3267.1986.

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Transcription of the heavy strand of mouse mitochondrial DNA starts from two closely spaced, distinct sites located in the displacement loop region of the genome. We report here an analysis of regulatory sequences required for faithful transcription from these two sites. Data obtained from in vitro assays demonstrated that a 51-base-pair region, encompassing nucleotides -40 to +11 of the downstream start site, contains sufficient information for accurate transcription from both start sites. Deletion of the 3' flanking sequences, including one or both start sites to -17, resulted in the initiation of transcription by the mitochondrial RNA polymerase from alternative sites within vector DNA sequences. This feature places the mouse heavy-strand promoter uniquely among other known mitochondrial promoters, all of which absolutely require cognate start sites for transcription. Comparison of the heavy-strand promoter with those of other vertebrate mitochondrial DNAs revealed a remarkably high rate of sequence divergence among species.

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Chang, D. D., and D. A. Clayton. "Precise assignment of the heavy-strand promoter of mouse mitochondrial DNA: cognate start sites are not required for transcriptional initiation." Molecular and Cellular Biology 6, no. 9 (September 1986): 3262–67. http://dx.doi.org/10.1128/mcb.6.9.3262.

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Transcription of the heavy strand of mouse mitochondrial DNA starts from two closely spaced, distinct sites located in the displacement loop region of the genome. We report here an analysis of regulatory sequences required for faithful transcription from these two sites. Data obtained from in vitro assays demonstrated that a 51-base-pair region, encompassing nucleotides -40 to +11 of the downstream start site, contains sufficient information for accurate transcription from both start sites. Deletion of the 3' flanking sequences, including one or both start sites to -17, resulted in the initiation of transcription by the mitochondrial RNA polymerase from alternative sites within vector DNA sequences. This feature places the mouse heavy-strand promoter uniquely among other known mitochondrial promoters, all of which absolutely require cognate start sites for transcription. Comparison of the heavy-strand promoter with those of other vertebrate mitochondrial DNAs revealed a remarkably high rate of sequence divergence among species.

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Grichnik, J. M., B. A. French, and R. J. Schwartz. "The chicken skeletal alpha-actin gene promoter region exhibits partial dyad symmetry and a capacity to drive bidirectional transcription." Molecular and Cellular Biology 8, no. 11 (November 1988): 4587–97. http://dx.doi.org/10.1128/mcb.8.11.4587-4597.1988.

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The chicken skeletal alpha-actin gene promoter region (-202 to -12) provides myogenic transcriptional specificity. This promoter contains partial dyad symmetry about an axis at nucleotide -108 and in transfection experiments is capable of directing transcription in a bidirectional manner. At least three different transcription initiation start sites, oriented toward upstream sequences, were mapped 25 to 30 base pairs from TATA-like regions. The opposing transcriptional activity was potentiated upon the deletion of sequences proximal to the alpha-actin transcription start site. Thus, sequences which serve to position RNA polymerase for alpha-actin transcription may allow, in their absence, the selection of alternative and reverse-oriented start sites. Nuclear runoff transcription assays of embryonic muscle indicated that divergent transcription may occur in vivo but with rapid turnover of nuclear transcripts. Divergent transcriptional activity enabled us to define the 3' regulatory boundary of the skeletal alpha-actin promoter which retains a high level of myogenic transcriptional activity. The 3' regulatory border was detected when serial 3' deletions bisected the element (-91 CCAAA TATGG -82) which reduced transcriptional activity by 80%. Previously we showed that disruption of its upstream counterpart (-127 CCAAAGAAGG -136) resulted in about a 90% decrease in activity. These element pairs, which we describe as CCAAT box-associated repeats, are conserved in all sequenced vertebrate sarcomeric actin genes and may act in a cooperative manner to facilitate transcription in myogenic cells.

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Grichnik, J. M., B. A. French, and R. J. Schwartz. "The chicken skeletal alpha-actin gene promoter region exhibits partial dyad symmetry and a capacity to drive bidirectional transcription." Molecular and Cellular Biology 8, no. 11 (November 1988): 4587–97. http://dx.doi.org/10.1128/mcb.8.11.4587.

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The chicken skeletal alpha-actin gene promoter region (-202 to -12) provides myogenic transcriptional specificity. This promoter contains partial dyad symmetry about an axis at nucleotide -108 and in transfection experiments is capable of directing transcription in a bidirectional manner. At least three different transcription initiation start sites, oriented toward upstream sequences, were mapped 25 to 30 base pairs from TATA-like regions. The opposing transcriptional activity was potentiated upon the deletion of sequences proximal to the alpha-actin transcription start site. Thus, sequences which serve to position RNA polymerase for alpha-actin transcription may allow, in their absence, the selection of alternative and reverse-oriented start sites. Nuclear runoff transcription assays of embryonic muscle indicated that divergent transcription may occur in vivo but with rapid turnover of nuclear transcripts. Divergent transcriptional activity enabled us to define the 3' regulatory boundary of the skeletal alpha-actin promoter which retains a high level of myogenic transcriptional activity. The 3' regulatory border was detected when serial 3' deletions bisected the element (-91 CCAAA TATGG -82) which reduced transcriptional activity by 80%. Previously we showed that disruption of its upstream counterpart (-127 CCAAAGAAGG -136) resulted in about a 90% decrease in activity. These element pairs, which we describe as CCAAT box-associated repeats, are conserved in all sequenced vertebrate sarcomeric actin genes and may act in a cooperative manner to facilitate transcription in myogenic cells.

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Geng, Y., and L. F. Johnson. "Lack of an initiator element is responsible for multiple transcriptional initiation sites of the TATA-less mouse thymidylate synthase promoter." Molecular and Cellular Biology 13, no. 8 (August 1993): 4894–903. http://dx.doi.org/10.1128/mcb.13.8.4894-4903.1993.

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The mouse thymidylate synthase promoter lacks a TATA box and initiates transcription at many sites across a 90-nucleotide initiation window. We showed previously that wild-type promoter activity is maintained with a promoter that extends only 13 nucleotides upstream of the first start site. G/A-rich and G/C-rich promoter elements were identified in the vicinity of the first transcriptional start site. The goals of the present study were to determine whether there are additional promoter elements in the initiation window and to determine why transcription initiates across such a broad region. Minigenes containing a variety of substitution, deletion, and insertion mutations in the promoter region were transfected into cultured cells, and the effects on expression and the pattern of start sites were determined. The results indicate that there are no additional promoter elements downstream of the G/C box. The boundaries of the transcription window are established by elements near the 5' end of the window, whereas the pattern of start sites is determined by sequences within the window. The promoter lacks an initiator element. When an initiator element was inserted, transcription initiated predominantly at the position directed by the initiator when it was inserted within the initiation window but not when it was inserted immediately upstream of the window.

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Geng, Y., and L. F. Johnson. "Lack of an initiator element is responsible for multiple transcriptional initiation sites of the TATA-less mouse thymidylate synthase promoter." Molecular and Cellular Biology 13, no. 8 (August 1993): 4894–903. http://dx.doi.org/10.1128/mcb.13.8.4894.

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The mouse thymidylate synthase promoter lacks a TATA box and initiates transcription at many sites across a 90-nucleotide initiation window. We showed previously that wild-type promoter activity is maintained with a promoter that extends only 13 nucleotides upstream of the first start site. G/A-rich and G/C-rich promoter elements were identified in the vicinity of the first transcriptional start site. The goals of the present study were to determine whether there are additional promoter elements in the initiation window and to determine why transcription initiates across such a broad region. Minigenes containing a variety of substitution, deletion, and insertion mutations in the promoter region were transfected into cultured cells, and the effects on expression and the pattern of start sites were determined. The results indicate that there are no additional promoter elements downstream of the G/C box. The boundaries of the transcription window are established by elements near the 5' end of the window, whereas the pattern of start sites is determined by sequences within the window. The promoter lacks an initiator element. When an initiator element was inserted, transcription initiated predominantly at the position directed by the initiator when it was inserted within the initiation window but not when it was inserted immediately upstream of the window.

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28

Nagai, Shigeki, Ralph E. Davis, Pierre Jean Mattei, Kyle Patrick Eagen, and Roger D. Kornberg. "Chromatin potentiates transcription." Proceedings of the National Academy of Sciences 114, no. 7 (January 30, 2017): 1536–41. http://dx.doi.org/10.1073/pnas.1620312114.

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Chromatin isolated from the chromosomal locus of the PHO5 gene of yeast in a transcriptionally repressed state was transcribed with 12 pure proteins (80 polypeptides): RNA polymerase II, six general transcription factors, TFIIS, the Pho4 gene activator protein, and the SAGA, SWI/SNF, and Mediator complexes. Contrary to expectation, a nucleosome occluding the TATA box and transcription start sites did not impede transcription but rather, enhanced it: the level of chromatin transcription was at least sevenfold greater than that of naked DNA, and chromatin gave patterns of transcription start sites closely similar to those occurring in vivo, whereas naked DNA gave many aberrant transcripts. Both histone acetylation and trimethylation of H3K4 (H3K4me3) were important for chromatin transcription. The nucleosome, long known to serve as a general gene repressor, thus also performs an important positive role in transcription.

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29

Hoshizaki, Johanna, and Marcus C. S. Lee. "Scientists on a RAMPAGE to find apicomplexan transcription start sites." Nature Reviews Microbiology 19, no. 8 (June 3, 2021): 483. http://dx.doi.org/10.1038/s41579-021-00587-8.

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30

Qin, Zhiyi, Peter Stoilov, Xuegong Zhang, and Yi Xing. "SEASTAR: systematic evaluation of alternative transcription start sites in RNA." Nucleic Acids Research 46, no. 8 (March 13, 2018): e45-e45. http://dx.doi.org/10.1093/nar/gky053.

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31

Schroeder, Diane I., and Richard M. Myers. "Multiple transcription start sites for FOXP2 with varying cellular specificities." Gene 413, no. 1-2 (April 2008): 42–48. http://dx.doi.org/10.1016/j.gene.2008.01.015.

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32

Xu, Chun-Fang, Melissa A. Brown, Julie A. Chambers, Beatrice Griffiths, Hans Nicolai, and Ellen Solomon. "Distinct transcription start sites generate two forms of BRCA1 mRNA." Human Molecular Genetics 4, no. 12 (1995): 2259–64. http://dx.doi.org/10.1093/hmg/4.12.2259.

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33

Kalosakas, G., K. Ø. Rasmussen, A. R. Bishop, C. H. Choi, and A. Usheva. "Sequence-specific thermal fluctuations identify start sites for DNA transcription." Europhysics Letters (EPL) 68, no. 1 (October 2004): 127–33. http://dx.doi.org/10.1209/epl/i2004-10167-8.

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34

Yamashita, R. "DBTSS: DataBase of Human Transcription Start Sites, progress report 2006." Nucleic Acids Research 34, no. 90001 (January 1, 2006): D86—D89. http://dx.doi.org/10.1093/nar/gkj129.

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35

Singh, Sandeep, Karol Szlachta, Arkadi Manukyan, Heather M. Raimer, Manikarna Dinda, Stefan Bekiranov, and Yuh-Hwa Wang. "Pausing sites of RNA polymerase II on actively transcribed genes are enriched in DNA double-stranded breaks." Journal of Biological Chemistry 295, no. 12 (February 6, 2020): 3990–4000. http://dx.doi.org/10.1074/jbc.ra119.011665.

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DNA double-stranded breaks (DSBs) are strongly associated with active transcription, and promoter-proximal pausing of RNA polymerase II (Pol II) is a critical step in transcriptional regulation. Mapping the distribution of DSBs along actively expressed genes and identifying the location of DSBs relative to pausing sites can provide mechanistic insights into transcriptional regulation. Using genome-wide DNA break mapping/sequencing techniques at single-nucleotide resolution in human cells, we found that DSBs are preferentially located around transcription start sites of highly transcribed and paused genes and that Pol II promoter-proximal pausing sites are enriched in DSBs. We observed that DSB frequency at pausing sites increases as the strength of pausing increases, regardless of whether the pausing sites are near or far from annotated transcription start sites. Inhibition of topoisomerase I and II by camptothecin and etoposide treatment, respectively, increased DSBs at the pausing sites as the concentrations of drugs increased, demonstrating the involvement of topoisomerases in DSB generation at the pausing sites. DNA breaks generated by topoisomerases are short-lived because of the religation activity of these enzymes, which these drugs inhibit; therefore, the observation of increased DSBs with increasing drug doses at pausing sites indicated active recruitment of topoisomerases to these sites. Furthermore, the enrichment and locations of DSBs at pausing sites were shared among different cell types, suggesting that Pol II promoter-proximal pausing is a common regulatory mechanism. Our findings support a model in which topoisomerases participate in Pol II promoter-proximal pausing and indicated that DSBs at pausing sites contribute to transcriptional activation.

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36

Park, J. H., and M. W. Taylor. "Analysis of signals controlling expression of the Chinese hamster ovary aprt gene." Molecular and Cellular Biology 8, no. 6 (June 1988): 2536–44. http://dx.doi.org/10.1128/mcb.8.6.2536-2544.1988.

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The 5' end of the Chinese hamster ovary aprt gene was sequenced and transcription start sites were determined by both S1 nuclease protection and primer extension assays. Deletion mutants covering the same area were constructed, and adenine phosphoribosyltransferase (APRT) or chloramphenicol acetyltransferase (CAT) activity was measured by transient-expression assays. The aprt gene uses a single cluster of transcription start sites and lacks consensus sequences such as TATA and CCAAT, which are general components of eucaryotic promoters. The 5' deletion mutations of the promoter sequences demonstrated that (i) there is no decrease in either APRT activity or transcription extending to position -89 (relative to the main transcription start site); (ii) an additional 29-base-pair (bp) deletion decreases APRT activity and transcription twofold; and (iii) a deletion past the transcription start sites (P5' delta +27) abolishes both APRT activity and transcription, indicating that a 60-bp fragment immediately upstream of the main transcription start site is involved in basic transcription and a 29-bp fragment just upstream of the 60 bp-fragment stimulates transcription twofold. The 3' deletion mutations showed that a deletion of a 61-bp fragment in the 5' leader and coding sequence abolishes the efficient translation of an aprt-CAT gene transcript. In addition, there are two polyadenylation signals at the genomic 3' end, with the proximal one being sufficient for functional polyadenylation.

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37

Park, J. H., and M. W. Taylor. "Analysis of signals controlling expression of the Chinese hamster ovary aprt gene." Molecular and Cellular Biology 8, no. 6 (June 1988): 2536–44. http://dx.doi.org/10.1128/mcb.8.6.2536.

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The 5' end of the Chinese hamster ovary aprt gene was sequenced and transcription start sites were determined by both S1 nuclease protection and primer extension assays. Deletion mutants covering the same area were constructed, and adenine phosphoribosyltransferase (APRT) or chloramphenicol acetyltransferase (CAT) activity was measured by transient-expression assays. The aprt gene uses a single cluster of transcription start sites and lacks consensus sequences such as TATA and CCAAT, which are general components of eucaryotic promoters. The 5' deletion mutations of the promoter sequences demonstrated that (i) there is no decrease in either APRT activity or transcription extending to position -89 (relative to the main transcription start site); (ii) an additional 29-base-pair (bp) deletion decreases APRT activity and transcription twofold; and (iii) a deletion past the transcription start sites (P5' delta +27) abolishes both APRT activity and transcription, indicating that a 60-bp fragment immediately upstream of the main transcription start site is involved in basic transcription and a 29-bp fragment just upstream of the 60 bp-fragment stimulates transcription twofold. The 3' deletion mutations showed that a deletion of a 61-bp fragment in the 5' leader and coding sequence abolishes the efficient translation of an aprt-CAT gene transcript. In addition, there are two polyadenylation signals at the genomic 3' end, with the proximal one being sufficient for functional polyadenylation.

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38

Sierra, F., G. H. Fey, and Y. Guigoz. "T-kininogen gene expression is induced during aging." Molecular and Cellular Biology 9, no. 12 (December 1989): 5610–16. http://dx.doi.org/10.1128/mcb.9.12.5610-5616.1989.

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We have constructed a cDNA library from senescent (24-month-old) rat liver mRNA and, by differential screening, have selected clones corresponding to mRNA species with increased abundance in aging rats. Direct sequencing of the inserts indicated that most of the clones (9 of 10) contained sequences coding for T-kininogen, also called major acute-phase protein, cysteine protease inhibitor, or thiostatin. Nuclear elongation experiments showed that the increase in mRNA concentration was controlled at the transcriptional level. RNase mapping and S1 analysis indicated that the age-dependent induction operated preferentially at one of the three transcriptional start sites of the gene(s). The acute-phase reaction (inflammation) is known to also induce these genes at the level of transcription; however, two of the three start sites are induced by inflammation. Transcription from one of these sites was induced by both phenomena, aging and inflammation.

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39

Sierra, F., G. H. Fey, and Y. Guigoz. "T-kininogen gene expression is induced during aging." Molecular and Cellular Biology 9, no. 12 (December 1989): 5610–16. http://dx.doi.org/10.1128/mcb.9.12.5610.

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We have constructed a cDNA library from senescent (24-month-old) rat liver mRNA and, by differential screening, have selected clones corresponding to mRNA species with increased abundance in aging rats. Direct sequencing of the inserts indicated that most of the clones (9 of 10) contained sequences coding for T-kininogen, also called major acute-phase protein, cysteine protease inhibitor, or thiostatin. Nuclear elongation experiments showed that the increase in mRNA concentration was controlled at the transcriptional level. RNase mapping and S1 analysis indicated that the age-dependent induction operated preferentially at one of the three transcriptional start sites of the gene(s). The acute-phase reaction (inflammation) is known to also induce these genes at the level of transcription; however, two of the three start sites are induced by inflammation. Transcription from one of these sites was induced by both phenomena, aging and inflammation.

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40

Perrin, David M., C. h. B. Chen, Yue Xu, Lori Pearson, and David S. Sigman. "Gene-Specific Transcription Inhibitors. Pentanucleotides Complementary to the Template Strand of Transcription Start Sites." Journal of the American Chemical Society 119, no. 24 (June 1997): 5746–47. http://dx.doi.org/10.1021/ja9634435.

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41

Wilson, G. L., V. Najfeld, E. Kozlow, J. Menniger, D. Ward, and J. H. Kehrl. "Genomic structure and chromosomal mapping of the human CD22 gene." Journal of Immunology 150, no. 11 (June 1, 1993): 5013–24. http://dx.doi.org/10.4049/jimmunol.150.11.5013.

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Abstract The human CD22 gene is expressed specifically in B lymphocytes and likely has an important function in cell-cell interactions. A nearly full length human CD22 cDNA clone was used to isolate genomic clones that span the CD22 gene. The CD22 gene is spread over 22 kb of DNA and is composed of 15 exons. The first exon contains the major transcriptional start sites. The translation initiation codon is located in exon 3, which also encodes a portion of the signal peptide. Exons 4 to 10 encode the seven Ig domains of CD22, exon 11 encodes the transmembrane domain, exons 12 to 15 encode the intracytoplasmic domain of CD22, and exon 15 also contains the 3' untranslated region. A minor form of CD22 mRNA likely results from splicing of exon 5 to exon 8, skipping exons 6 and 7. A 4.6-kb XbaI fragment of the CD22 gene was used to map the chromosomal location of CD22 by fluorescence in situ hybridization. The hybridization locus was identified by combining fluorescent images of the probe with the chromosomal banding pattern generated by an Alu probe. The results demonstrate that CD22 is located within the band region q13.1 of chromosome 19. Two closely clustered major transcription start sites and several minor start sites were mapped by primer extension. Similarly to many other lymphoid-specific genes, the CD22 promoter lacks an obvious TATA box. Approximately 4 kb of DNA 5' of the transcription start sites were sequenced and found to contain multiple Alu elements. Potential binding sites for the transcriptional factors NF-kappa B, AP-1, and Oct-2 are located within 300 bp 5' of the major transcription start sites. A 400-bp fragment (bp -339 through +71) of the CD22 promoter region was subcloned into a pGEM-chloramphenicol acetyltransferase vector and after transfection into B and T cells was found to be active in both B and T cells. Further studies of the CD22 gene should lead to a greater understanding of the expression of CD22 during B cell development and differentiation.

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42

Soldati, D., and J. C. Boothroyd. "A selector of transcription initiation in the protozoan parasite Toxoplasma gondii." Molecular and Cellular Biology 15, no. 1 (January 1995): 87–93. http://dx.doi.org/10.1128/mcb.15.1.87.

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The recent development of an efficient transfection system for the apicomplexan Toxoplasma gondii allows a comprehensive dissection of the elements involved in gene transcription in this obligate intracellular parasite. We demonstrate here that for the SAG1 gene, a stretch of six repeated sequences in the region 35 to 190 bp upstream of the first of two transcription start sites is essential for efficient and accurate transcription initiation. This repeat element shows characteristics of a selector in determining the position of the transcription start sites.

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43

Lee, S., and D. S. Greenspan. "Transcriptional promoter of the human α1(V) collagen gene (COL5A1)." Biochemical Journal 310, no. 1 (August 15, 1995): 15–22. http://dx.doi.org/10.1042/bj3100015.

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We have characterized the 5′ region of the human alpha 1(V) collagen gene (COL5A1). The transcriptional promoter is shown to have a number of features characteristic of the promoters of ‘housekeeping’ and growth-control-related genes. It lacks obvious TATA and CAAT boxes, has multiple transcription start sites, has a high GC content, lies within a well-defined CpG island and has a number of consensus sites for the potential binding of transcription factor Sp1. This type of promoter structure, while unusual for a collagen gene, is consistent with the broad distribution of expression of COL5A1 and is reminiscent of the promoter structures of the genes encoding type VI collagen, which has a similarly broad distribution of expression. Stepwise deletion of COL5A1 5′ sequences, placed upstream of a heterologous reporter gene, yielded a gradual decrease in promoter activity, indicating that the COL5A1 promoter is composed of an array of cis-acting elements. A minimal promoter region contained within the 212 bp immediately upstream of the major transcription start site contained no consensus sequences for the binding of known transcription factors, but gel mobility shift assays showed this region to bind nuclear factors, including Sp1, at a number of sites. The major transcription start site is flanked by an upstream 34-bp oligopurine/oligopyrimidine stretch, or ‘GAGA’ box, and a downstream 56-bp GAGA box which contains a 10-bp mirror repeat and is sensitive to cleavage with S1 nuclease.

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44

Mitchell, P. J., A. M. Carothers, J. H. Han, J. D. Harding, E. Kas, L. Venolia, and L. A. Chasin. "Multiple transcription start sites, DNase I-hypersensitive sites, and an opposite-strand exon in the 5' region of the CHO dhfr gene." Molecular and Cellular Biology 6, no. 2 (February 1986): 425–40. http://dx.doi.org/10.1128/mcb.6.2.425-440.1986.

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Transcription of the 26-kilobase (kb) dihydrofolate reductase (dhfr) gene in CHO cells is initiated at two sites: a major site (approximately 85% of the dhfr mRNA) at -63 relative to the translation start and a minor site (approximately 15%) at -107. Transcription also occurs from the opposite DNA strand in the dhfr 5' region, with a probable initiation site at approximately -195 relative to the dhfr translation start. A 4-kb polyadenylated RNA that is derived from the opposite-strand transcription increases threefold in abundance after serum starvation of CHO cells for 24 h. dhfr mRNA levels do not change during this time. The first dhfr exon lies within a 1-kb genomic region marked by exceptionally high G + C content and lack of DNA methylation. This region also includes a 214-base-pair (bp) exon for the opposite-strand transcript and five of the six DNase I-hypersensitive sites identified at the dhfr locus. Analysis of the DNA sequences of hamster, human (M. Chen, T. Shimada, A. D. Moulton, A. Cline, R. K. Humphries, J. Maizel, and A. W. Nienhuis, J. Biol. Chem. 259:3933-3943, 1984), and mouse (M. McGrogan, C. C. Simonsen, D. T. Smouse, P. J. Farnham, and R. T. Schimke, J. Biol. Chem. 260:2307-2314, 1985) dhfr genes reveals the presence of a 29-bp unit that is conserved 45 to 49 bp upstream of major and minor dhfr transcription start sites. This unit follows the consensus: GRGGCGGTGGCCTNNNNTGTCRCAARTRGGTR. The 5' part of the 29-bp unit contains a GC box that agrees with the GGGCGG consensus-binding site for the RNA polymerase II transcription factor Sp1 (D. Gidoni, W. A. Dynan, and R. Tjian, Nature (London) 312:409-413, 1984). Each of the three mammalian dhfr genes has several G-rich GC boxes proximal to the major dhfr transcription start site and several GC boxes of the opposite orientation (C rich) in a distal region about 500 bp upstream.

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45

Mitchell, P. J., A. M. Carothers, J. H. Han, J. D. Harding, E. Kas, L. Venolia, and L. A. Chasin. "Multiple transcription start sites, DNase I-hypersensitive sites, and an opposite-strand exon in the 5' region of the CHO dhfr gene." Molecular and Cellular Biology 6, no. 2 (February 1986): 425–40. http://dx.doi.org/10.1128/mcb.6.2.425.

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Transcription of the 26-kilobase (kb) dihydrofolate reductase (dhfr) gene in CHO cells is initiated at two sites: a major site (approximately 85% of the dhfr mRNA) at -63 relative to the translation start and a minor site (approximately 15%) at -107. Transcription also occurs from the opposite DNA strand in the dhfr 5' region, with a probable initiation site at approximately -195 relative to the dhfr translation start. A 4-kb polyadenylated RNA that is derived from the opposite-strand transcription increases threefold in abundance after serum starvation of CHO cells for 24 h. dhfr mRNA levels do not change during this time. The first dhfr exon lies within a 1-kb genomic region marked by exceptionally high G + C content and lack of DNA methylation. This region also includes a 214-base-pair (bp) exon for the opposite-strand transcript and five of the six DNase I-hypersensitive sites identified at the dhfr locus. Analysis of the DNA sequences of hamster, human (M. Chen, T. Shimada, A. D. Moulton, A. Cline, R. K. Humphries, J. Maizel, and A. W. Nienhuis, J. Biol. Chem. 259:3933-3943, 1984), and mouse (M. McGrogan, C. C. Simonsen, D. T. Smouse, P. J. Farnham, and R. T. Schimke, J. Biol. Chem. 260:2307-2314, 1985) dhfr genes reveals the presence of a 29-bp unit that is conserved 45 to 49 bp upstream of major and minor dhfr transcription start sites. This unit follows the consensus: GRGGCGGTGGCCTNNNNTGTCRCAARTRGGTR. The 5' part of the 29-bp unit contains a GC box that agrees with the GGGCGG consensus-binding site for the RNA polymerase II transcription factor Sp1 (D. Gidoni, W. A. Dynan, and R. Tjian, Nature (London) 312:409-413, 1984). Each of the three mammalian dhfr genes has several G-rich GC boxes proximal to the major dhfr transcription start site and several GC boxes of the opposite orientation (C rich) in a distal region about 500 bp upstream.

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46

Jones, Peter A. "Decoding the Chromatin Code." Blood 120, no. 21 (November 16, 2012): SCI—4—SCI—4. http://dx.doi.org/10.1182/blood.v120.21.sci-4.sci-4.

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Abstract Abstract SCI-4 Epigenetic processes are reinforced by interactions between covalent chromatin marks such as DNA methylation, histone modifications, and variants thereof. These marks ultimately specify the locations of nucleosomes, particularly with respect to transcriptional start sites and other regulatory regions. Understanding how the epigenome functions, therefore, requires a coordinated approach in order to reveal the mechanisms by which the chemical modifications interact with nucleosomal remodeling machines to ensure epigenetic inheritance and control of gene expression. We have developed a new methodology to simultaneously map nucleosomal positioning and DNA methylation on individual molecules of DNA. We used this nucleosomal mapping technology to ascertain alterations in nucleosomal positioning during the abnormal silencing of genes by promoter hypermethylation. These experiments show that the methylation of CpG islands at the transcriptional start sites of key tumor-suppressor genes results in the stable placement of nucleosomes at the transcription start site. Treatment with 5-azanucleoside results in an immediate inhibition of DNA methylation and a sequence of downstream events that ultimately result in the eviction of the nucleosomes from the transcription start site and the activation of gene expression. Disclosures: Jones: Eli Lilly: Consultancy.

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47

Blake, M. C., R. C. Jambou, A. G. Swick, J. W. Kahn, and J. C. Azizkhan. "Transcriptional initiation is controlled by upstream GC-box interactions in a TATAA-less promoter." Molecular and Cellular Biology 10, no. 12 (December 1990): 6632–41. http://dx.doi.org/10.1128/mcb.10.12.6632-6641.1990.

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Numerous genes contain TATAA-less promoters, and the control of transcriptional initiation in this important promoter class is not understood. We have determined that protein-DNA interactions at three of the four proximal GC box sequence elements in one such promoter, that of the hamster dihydrofolate reductase gene, control initiation and relative use of the major and minor start sites. Our results indicate that although the GC boxes are apparently equivalent with respect to factor binding, they are not equivalent with respect to function. At least two properly positioned GC boxes were required for initiation of transcription. Abolishment of DNA-protein interaction by site-specific mutation of the most proximal GC box (box I) resulted in a fivefold decrease in transcription from the major initiation site and a threefold increase in heterogeneous transcripts initiating from the vicinity of the minor start site in vitro and in vivo. Mutations that separately abolished interactions at GC boxes II and III while leaving GC box I intact affected the relative utilization of both the major and minor initiation sites as well as transcriptional efficiency of the promoter template in in vitro transcription and transient expression assays. Interaction at GC box IV when the three proximal boxes were in a wild-type configuration had no effect on transcription of the dihydrofolate reductase gene promoter. Thus, GC box interactions not only are required for efficient transcription but also regulate start site utilization in this TATAA-less promoter.

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48

Blake, M. C., R. C. Jambou, A. G. Swick, J. W. Kahn, and J. C. Azizkhan. "Transcriptional initiation is controlled by upstream GC-box interactions in a TATAA-less promoter." Molecular and Cellular Biology 10, no. 12 (December 1990): 6632–41. http://dx.doi.org/10.1128/mcb.10.12.6632.

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Numerous genes contain TATAA-less promoters, and the control of transcriptional initiation in this important promoter class is not understood. We have determined that protein-DNA interactions at three of the four proximal GC box sequence elements in one such promoter, that of the hamster dihydrofolate reductase gene, control initiation and relative use of the major and minor start sites. Our results indicate that although the GC boxes are apparently equivalent with respect to factor binding, they are not equivalent with respect to function. At least two properly positioned GC boxes were required for initiation of transcription. Abolishment of DNA-protein interaction by site-specific mutation of the most proximal GC box (box I) resulted in a fivefold decrease in transcription from the major initiation site and a threefold increase in heterogeneous transcripts initiating from the vicinity of the minor start site in vitro and in vivo. Mutations that separately abolished interactions at GC boxes II and III while leaving GC box I intact affected the relative utilization of both the major and minor initiation sites as well as transcriptional efficiency of the promoter template in in vitro transcription and transient expression assays. Interaction at GC box IV when the three proximal boxes were in a wild-type configuration had no effect on transcription of the dihydrofolate reductase gene promoter. Thus, GC box interactions not only are required for efficient transcription but also regulate start site utilization in this TATAA-less promoter.

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49

Huang, Yongsheng, Kajal Sitwala, Joel Bronstein, Daniel Sanders, Monisha Dandekar, Cailin Collins, Gordon Robertson, et al. "Identification and characterization of Hoxa9 binding sites in hematopoietic cells." Blood 119, no. 2 (January 12, 2012): 388–98. http://dx.doi.org/10.1182/blood-2011-03-341081.

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The clustered homeobox proteins play crucial roles in development, hematopoiesis, and leukemia, yet the targets they regulate and their mechanisms of action are poorly understood. Here, we identified the binding sites for Hoxa9 and the Hox cofactor Meis1 on a genome-wide level and profiled their associated epigenetic modifications and transcriptional targets. Hoxa9 and the Hox cofactor Meis1 cobind at hundreds of highly evolutionarily conserved sites, most of which are distant from transcription start sites. These sites show high levels of histone H3K4 monomethylation and CBP/P300 binding characteristic of enhancers. Furthermore, a subset of these sites shows enhancer activity in transient transfection assays. Many Hoxa9 and Meis1 binding sites are also bound by PU.1 and other lineage-restricted transcription factors previously implicated in establishment of myeloid enhancers. Conditional Hoxa9 activation is associated with CBP/P300 recruitment, histone acetylation, and transcriptional activation of a network of proto-oncogenes, including Erg, Flt3, Lmo2, Myb, and Sox4. Collectively, this work suggests that Hoxa9 regulates transcription by interacting with enhancers of genes important for hematopoiesis and leukemia.

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Healy, A. M., T. L. Helser, and R. S. Zitomer. "Sequences required for transcriptional initiation of the Saccharomyces cerevisiae CYC7 genes." Molecular and Cellular Biology 7, no. 10 (October 1987): 3785–91. http://dx.doi.org/10.1128/mcb.7.10.3785-3791.1987.

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A series of BAL 31 deletions were constructed in the upstream region of the Saccharomyces cerevisiae CYC7 gene to determine sequences required for transcriptional initiation. These deletions identified the TATA box as an alternating A-T sequence at -160 and the initiation sequences as well as the spatial relationship between them. The TATA box was necessary for wild-type levels of expression of the CYC7 gene. Decreasing the distance between the TATA sequence and the initiation site did not alter gene expression, but the site of transcription was shifted 3'-ward. In most cases, transcription initiated at a number of sites, the 5'-most of which was the first suitable site greater than 45 base pairs 3' of the TATA sequence, suggesting a spatial relationship between these sequences. Consensus sequences previously proposed for initiation sites were evaluated with respect to the start sites identified in this study as well as the start sites of other yeast genes.

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Journal articles on the topic 'Transcription Start Sites'

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