Journal articles: 'Transcriptional interference'

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O’Callaghan, Chris, Da Lin, and Thomas K. Hiron. "Intragenic transcriptional interference regulates the human immune ligand MICA." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 109.23. http://dx.doi.org/10.4049/jimmunol.200.supp.109.23.

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Abstract Regulation of MICA expression is incompletely understood, but human MICA can be upregulated in cancer cells, virus-infected cells and rapidly proliferating cells. Binding of MICA to the activating NKG2D receptor on cytotoxic immune cells promotes elimination of the cell expressing MICA. We noted that MICA has tandem promoters that drive overlapping forward transcription. We show that the MICA gene contains a conserved upstream promoter that expresses a non coding transcript. Transcription from the upstream promoter represses transcription from the standard downstream MICA promoter in cis through transcriptional interference. The effect of transcriptional interference depends on the strength of transcription from the upstream promoter and quantitative studies show that it is described by a simple reciprocal repressor function. The time course of transcriptional interference coincides with recruitment at the standard downstream promoter of factors involved in nucleosomal remodeling during transcription. Transcriptional interference is demonstrated in the regulation of MICA expression by the physiological inputs interferon-γ and interleukin-4, that both act through regulatory DNA elements in the upstream promoter. These findings have significant implications for the understanding of MICA expression. Transcription factors activating the downstream promoter will upregulate MICA expression, whereas transcription factors activating the upstream promoter will downregulated MICA expression. A genome-wide analysis indicates that transcriptional interference between tandem intragenic promoters may be involved in regulating the expression of multiple other human genes.

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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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Ingelbrecht, I., P. Breyne, K. Vancompernolle, A. Jacobs, M. Van Montagu, and A. Depicker. "Transcriptional interference in transgenic plants." Gene 109, no. 2 (December 1991): 239–42. http://dx.doi.org/10.1016/0378-1119(91)90614-h.

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4

SHEARWIN, K., B. CALLEN, and J. EGAN. "Transcriptional interference – a crash course." Trends in Genetics 21, no. 6 (June 2005): 339–45. http://dx.doi.org/10.1016/j.tig.2005.04.009.

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Hu, Xiao, Susan Eszterhas, Nicolas Pallazzi, Eric E. Bouhassira, Jennifer Fields, Osamu Tanabe, Scott A. Gerber, et al. "Transcriptional interference among the murine β-like globin genes." Blood 109, no. 5 (October 31, 2006): 2210–16. http://dx.doi.org/10.1182/blood-2006-06-029868.

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Abstract Mammalian β-globin loci contain multiple genes that are activated at different developmental stages. Studies have suggested that the transcription of one gene in a locus can influence the expression of the other locus genes. The prevalent model to explain this transcriptional interference is that all potentially active genes compete for locus control region (LCR) activity. To investigate the influence of transcription by the murine embryonic genes on transcription of the other β-like genes, we generated mice with deletions of the promoter regions of Ey and βh1 and measured transcription of the remaining genes. Deletion of the Ey and βh1 promoters increased transcription of βmajor and βminor 2-fold to 3-fold during primitive erythropoiesis. Deletion of Ey did not affect βh1 nor did deletion of βh1 affect Ey, but Ey deletion uniquely activated transcription from βh0, a β-like globin gene immediately downstream of Ey. Protein analysis showed that βh0 encodes a translatable β-like globin protein that can pair with alpha globin. The lack of transcriptional interference between Ey and βh1 and the gene-specific repression of βh0 did not support LCR competition among the embryonic genes and suggested that direct transcriptional interference from Ey suppressed βh0.

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Palmer, Adam C., J. Barry Egan, and Keith E. Shearwin. "Transcriptional interference by RNA polymerase pausing and dislodgement of transcription factors." Transcription 2, no. 1 (January 2011): 9–14. http://dx.doi.org/10.4161/trns.2.1.13511.

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7

Ard, Ryan, and Robin C. Allshire. "Transcription-coupled changes to chromatin underpin gene silencing by transcriptional interference." Nucleic Acids Research 44, no. 22 (September 8, 2016): 10619–30. http://dx.doi.org/10.1093/nar/gkw801.

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8

Chan, H., S. Hartung, and M. Breindl. "Retrovirus-induced interference with collagen I gene expression in Mov13 fibroblasts is maintained in the absence of DNA methylation." Molecular and Cellular Biology 11, no. 1 (January 1991): 47–54. http://dx.doi.org/10.1128/mcb.11.1.47-54.1991.

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We have studied the role of DNA methylation in repression of the murine alpha 1 type I collagen (COL1A1) gene in Mov13 fibroblasts. In Mov13 mice, a retroviral provirus has inserted into the first intron of the COL1A1 gene and blocks its expression at the level of transcriptional initiation. We found that regulatory sequences in the COL1A1 promoter region that are involved in the tissue-specific regulation of the gene are unmethylated in collagen-expressing wild-type fibroblasts and methylated in Mov13 fibroblasts, confirming and extending earlier observations. To directly assess the role of DNA methylation in the repression of COL1A1 gene transcription, we treated Mov13 fibroblasts with the demethylating agent 5-azacytidine. This treatment resulted in a demethylation of the COL1A1 regulatory sequences but failed to activate transcription of the COL1A1 gene. Moreover, the 5-azacytidine treatment induced a transcription-competent chromatin structure in the retroviral sequences but not in the COL1A1 promoter. In DNA transfection and microinjection experiments, we found that the provirus interfered with transcriptional activity of the COL1A1 promoter in Mov13 fibroblasts but not in Xenopus laevis oocytes. In contrast, the wild-type COL1A1 promoter was transcriptionally active in Mov13 fibroblasts. These experiments showed that the COL1A1 promoter is potentially transcriptionally active in the presence of proviral sequences and that Mov13 fibroblasts contain the trans-acting factors required for efficient COL1A1 gene expression. Our results indicate that the provirus insertion in Mov13 can inactivate COL1A1 gene expression at several levels. It prevents the developmentally regulated establishment of a transcription-competent methylation pattern and chromatin structure of the COL1A1 domain and, in the absence of DNA methylation, appears to suppress the COL1A1 promoter in a cell-specific manner, presumably by assuming a dominant chromatin structure that may be incompatible with transcriptional activity of flanking cellular sequences.

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Chan, H., S. Hartung, and M. Breindl. "Retrovirus-induced interference with collagen I gene expression in Mov13 fibroblasts is maintained in the absence of DNA methylation." Molecular and Cellular Biology 11, no. 1 (January 1991): 47–54. http://dx.doi.org/10.1128/mcb.11.1.47.

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We have studied the role of DNA methylation in repression of the murine alpha 1 type I collagen (COL1A1) gene in Mov13 fibroblasts. In Mov13 mice, a retroviral provirus has inserted into the first intron of the COL1A1 gene and blocks its expression at the level of transcriptional initiation. We found that regulatory sequences in the COL1A1 promoter region that are involved in the tissue-specific regulation of the gene are unmethylated in collagen-expressing wild-type fibroblasts and methylated in Mov13 fibroblasts, confirming and extending earlier observations. To directly assess the role of DNA methylation in the repression of COL1A1 gene transcription, we treated Mov13 fibroblasts with the demethylating agent 5-azacytidine. This treatment resulted in a demethylation of the COL1A1 regulatory sequences but failed to activate transcription of the COL1A1 gene. Moreover, the 5-azacytidine treatment induced a transcription-competent chromatin structure in the retroviral sequences but not in the COL1A1 promoter. In DNA transfection and microinjection experiments, we found that the provirus interfered with transcriptional activity of the COL1A1 promoter in Mov13 fibroblasts but not in Xenopus laevis oocytes. In contrast, the wild-type COL1A1 promoter was transcriptionally active in Mov13 fibroblasts. These experiments showed that the COL1A1 promoter is potentially transcriptionally active in the presence of proviral sequences and that Mov13 fibroblasts contain the trans-acting factors required for efficient COL1A1 gene expression. Our results indicate that the provirus insertion in Mov13 can inactivate COL1A1 gene expression at several levels. It prevents the developmentally regulated establishment of a transcription-competent methylation pattern and chromatin structure of the COL1A1 domain and, in the absence of DNA methylation, appears to suppress the COL1A1 promoter in a cell-specific manner, presumably by assuming a dominant chromatin structure that may be incompatible with transcriptional activity of flanking cellular sequences.

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10

Jorgensen, Victoria, Jingxun Chen, Helen Vander Wende, Devon E. Harris, Alicia McCarthy, Shane Breznak, Siu Wah Wong-Deyrup, et al. "Tunable Transcriptional Interference at the Endogenous Alcohol Dehydrogenase Gene Locus in Drosophila melanogaster." G3: Genes|Genomes|Genetics 10, no. 5 (March 25, 2020): 1575–83. http://dx.doi.org/10.1534/g3.119.400937.

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Neighboring sequences of a gene can influence its expression. In the phenomenon known as transcriptional interference, transcription at one region in the genome can repress transcription at a nearby region in cis. Transcriptional interference occurs at a number of eukaryotic loci, including the alcohol dehydrogenase (Adh) gene in Drosophila melanogaster. Adh is regulated by two promoters, which are distinct in their developmental timing of activation. It has been shown using transgene insertion that when the promoter distal from the Adh start codon is deleted, transcription from the proximal promoter becomes de-regulated. As a result, the Adh proximal promoter, which is normally active only during the early larval stages, becomes abnormally activated in adults. Whether this type of regulation occurs in the endogenous Adh context, however, remains unclear. Here, we employed the CRISPR/Cas9 system to edit the endogenous Adh locus and found that removal of the distal promoter also resulted in the untimely expression of the proximal promoter-driven mRNA isoform in adults, albeit at lower levels than previously reported. Importantly, transcription from the distal promoter was sufficient to repress proximal transcription in larvae, and the degree of this repression was dependent on the degree of distal promoter activity. Finally, upregulation of the distal Adh transcript led to the enrichment of histone 3 lysine 36 trimethylation over the Adh proximal promoter. We conclude that the endogenous Adh locus is developmentally regulated by transcriptional interference in a tunable manner.

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11

Fogagnolo, Carolinne T., Daniela S. Mizobuti, and Marcio C. Bajgelman. "Abstract A010: Assay development to assess the efficiency and stability of candidate molecules for transcriptional gene silencing of FOXP3, using a human tumor-derived cell line." Cancer Immunology Research 11, no. 12_Supplement (December 1, 2023): A010. http://dx.doi.org/10.1158/2326-6074.tumimm23-a010.

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Abstract Regulatory T cells play an important role to modulate the balance between immunotolerance and immunosurveillance. These cells have the property of inhibiting effector lymphocytes and may antagonize antitumor immunity. Regulatory T cells are originated in the thymus, or even converted from peripheral lymphocytes by factors produced in the tumor microenvironment. Clinical data suggests that regulatory T cell infiltration correlates with poor prognosis in the treatment of solid tumors. The FOXP3 transcription factor is considered a master key to control the phenotype of regulatory T cells. It was previously shown, that the ectopic expression of FOXP3 can induce an immunosuppressive phenotype in lymphocytes. In contrast, it has been observed that mutations in the FOXP3 gene can cause impaired immunosuppressive activity mediated by regulatory T cells, such as the autoimmunity syndrome known as IPEX. In this sense, the FOXP3 transcription factor may be an interesting target, looking for inactivation of the immunosuppressive phenotype of regulatory T cells, to potentiate antitumor response. In this work, we present an assay development to investigate the potential of transcriptional interference RNA candidates to silence FOXP3 expression. In contrast to post-transcriptional gene silencing method, which targets messenger RNA and depends on a constant supply or efficient turn-over of the inhibitory molecule, the transcriptional gene silencing targets the cellular DNA genome, inducing epigenetic changes that may control the target gene transcription. We employed the human MCF-7 tumor cell line, which has endogenous and constitutive expression of FOXP3 as a target model to test transcriptional gene silencing candidates. This cell line is transduced with lentiviral vectors harboring interfering RNA sequences driven to the FOXP3 promoter region. The RNA interference candidates are then evaluated for their ability to induce DNA methylation, by bisulfite method, and transcriptional gene silencing of FOXP3, by qPCR. We performed the screening of candidates for FOXP3 transcriptional silencing, in comparison to a post-transcriptional interference RNA control. The lentiviral transduced cells are easily expanded and allow a temporal analysis of target gene expression. In this model, we observed the possibility of finding transcriptional interference RNA candidates that exhibited high efficiency and stability, that may be used for research purposes, or even for the investigation of new therapeutic possibilities in immuno-oncology. Citation Format: Carolinne T Fogagnolo, Daniela S Mizobuti, Marcio C Bajgelman. Assay development to assess the efficiency and stability of candidate molecules for transcriptional gene silencing of FOXP3, using a human tumor-derived cell line [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Tumor Immunology and Immunotherapy; 2023 Oct 1-4; Toronto, Ontario, Canada. Philadelphia (PA): AACR; Cancer Immunol Res 2023;11(12 Suppl):Abstract nr A010.

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12

Karin, M., and L. Chang. "AP-1--glucocorticoid receptor crosstalk taken to a higher level." Journal of Endocrinology 169, no. 3 (June 1, 2001): 447–51. http://dx.doi.org/10.1677/joe.0.1690447.

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More than a decade ago our view of gene regulation by glucocorticoids (GC) and other steroid hormones underwent a dramatic change with the discovery of negative crosstalk (transcriptional interference) between the GC receptor (GCR) and transcription factor AP-1 (Jun:Fos). It was initially observed that induction of the collagenase type 1 gene, which is mediated through activation of AP-1 by growth factors and inflammatory cytokines, is repressed by GC. This repression was attributed to mutual negative interactions between AP-1 and GCR. Although the exact molecular mechanism underlying this particular case of transcriptional interference is yet to be determined, it has become clear that this and analogous interactions with other transcription factors (e.g. nuclear factor-kappaB) underlie the anti-inflammatory and immunosuppressive activity of GC. Recent studies conducted at the whole animal level indicate that the interactions between the AP-1 and GC signaling pathways are much more extensive. AP-1-related signaling via the Jun N-terminal kinases can lead to increased levels of circulating GC, which eventually down-modulate AP-1 activity via transcriptional interference. This negative feedback loop is likely to be of great importance for maintenance of homeostasis and regulation of stress responses, including acute and chronic inflammation.

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Buetti‐Dinh, Antoine, Rosemarie Ungricht, János Z. Kelemen, Chetak Shetty, Prasuna Ratna, and Attila Becskei. "Control and signal processing by transcriptional interference." Molecular Systems Biology 5, no. 1 (January 2009): 300. http://dx.doi.org/10.1038/msb.2009.61.

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14

Saatcioglu, F., P. Bartunek, T. Deng, M. Zenke, and M. Karin. "A conserved C-terminal sequence that is deleted in v-ErbA is essential for the biological activities of c-ErbA (the thyroid hormone receptor)." Molecular and Cellular Biology 13, no. 6 (June 1993): 3675–85. http://dx.doi.org/10.1128/mcb.13.6.3675-3685.1993.

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The thyroid hormone (T3) receptor type alpha, the c-ErbA alpha proto-oncoprotein, stimulates transcription of T3-dependent promoters, interferes with AP-1 activity, and induces erythroid differentiation in a ligand-dependent manner. The v-ErbA oncoprotein does not bind hormone and has lost all of these activities. Using c-ErbA/v-ErbA chimeras, we found that a deletion of 9 amino acids, conserved among many members of the nuclear receptor superfamily, which are located at the extreme carboxy terminus of c-ErbA alpha is responsible for loss of both transactivation and transcriptional interference activities. Single, double, and triple amino acid substitutions within this region completely abolished T3-dependent transcriptional activation, interference with AP-1 activity, and decreased T3 binding by c-ErbA alpha. However, the lower T3 binding by these mutants does not fully account for the loss of transactivation and transcriptional interference, since a c-ErbA/v-ErbA chimera which was similarly reduced in T3 binding activity has retained both of these functions. Deletion of homologous residues in the retinoic acid receptor alpha (RAR alpha) resulted in a similar loss of transactivation and transcriptional interference activities. The ability of c-ErbA alpha to induce differentiation of transformed erythroblasts is also impaired by all of the mutations introduced into the conserved carboxy-terminal sequence. We conclude that this 9-amino-acid conserved region is essential for normal biological function of c-ErbA alpha and RAR alpha and possibly other T3 and RA receptors.

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Saatcioglu, F., P. Bartunek, T. Deng, M. Zenke, and M. Karin. "A conserved C-terminal sequence that is deleted in v-ErbA is essential for the biological activities of c-ErbA (the thyroid hormone receptor)." Molecular and Cellular Biology 13, no. 6 (June 1993): 3675–85. http://dx.doi.org/10.1128/mcb.13.6.3675.

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The thyroid hormone (T3) receptor type alpha, the c-ErbA alpha proto-oncoprotein, stimulates transcription of T3-dependent promoters, interferes with AP-1 activity, and induces erythroid differentiation in a ligand-dependent manner. The v-ErbA oncoprotein does not bind hormone and has lost all of these activities. Using c-ErbA/v-ErbA chimeras, we found that a deletion of 9 amino acids, conserved among many members of the nuclear receptor superfamily, which are located at the extreme carboxy terminus of c-ErbA alpha is responsible for loss of both transactivation and transcriptional interference activities. Single, double, and triple amino acid substitutions within this region completely abolished T3-dependent transcriptional activation, interference with AP-1 activity, and decreased T3 binding by c-ErbA alpha. However, the lower T3 binding by these mutants does not fully account for the loss of transactivation and transcriptional interference, since a c-ErbA/v-ErbA chimera which was similarly reduced in T3 binding activity has retained both of these functions. Deletion of homologous residues in the retinoic acid receptor alpha (RAR alpha) resulted in a similar loss of transactivation and transcriptional interference activities. The ability of c-ErbA alpha to induce differentiation of transformed erythroblasts is also impaired by all of the mutations introduced into the conserved carboxy-terminal sequence. We conclude that this 9-amino-acid conserved region is essential for normal biological function of c-ErbA alpha and RAR alpha and possibly other T3 and RA receptors.

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Hao, Nan, Adam C. Palmer, Ian B. Dodd, and Keith E. Shearwin. "Directing traffic on DNA—How transcription factors relieve or induce transcriptional interference." Transcription 8, no. 2 (March 1, 2017): 120–25. http://dx.doi.org/10.1080/21541264.2017.1285851.

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Schwer, Beate, Angad Garg, Agata Jacewicz, and Stewart Shuman. "Genetic screen for suppression of transcriptional interference identifies a gain-of-function mutation in Pol2 termination factor Seb1." Proceedings of the National Academy of Sciences 118, no. 33 (August 13, 2021): e2108105118. http://dx.doi.org/10.1073/pnas.2108105118.

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The system of long noncoding RNA (lncRNA)–mediated transcriptional interference that represses fission yeast phosphate homoeostasis gene pho1 provides a sensitive readout of genetic influences on cotranscriptional 3′-processing and termination and a tool for discovery of regulators of this phase of the Pol2 transcription cycle. Here, we conducted a genetic screen for relief of transcriptional interference that unveiled a mechanism by which Pol2 termination is enhanced via a gain-of-function mutation, G476S, in the RNA-binding domain of an essential termination factor, Seb1. The genetic and physical evidence for gain-of-function is compelling: 1) seb1-G476S de-represses pho1 and tgp1, both of which are subject to lncRNA-mediated transcriptional interference; 2) seb1-G476S elicits precocious lncRNA transcription termination in response to lncRNA 5′-proximal poly(A) signals; 3) seb1-G476S derepression of pho1 is effaced by loss-of-function mutations in cleavage and polyadenylation factor (CPF) subunits and termination factor Rhn1; 4) synthetic lethality of seb1-G476S with pho1 derepressive mutants rpb1-CTD-S7A and aps1∆ is rescued by CPF/Rhn1 loss-of-function alleles; and 5) seb1-G476S elicits an upstream shift in poly(A) site preference in several messenger RNA genes. A crystal structure of the Seb1-G476S RNA-binding domain indicates potential for gain of contacts from Ser476 to RNA nucleobases. To our knowledge, this is a unique instance of a gain-of-function phenotype in a eukaryal transcription termination protein.

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Snyder, M., R. J. Sapolsky, and R. W. Davis. "Transcription interferes with elements important for chromosome maintenance in Saccharomyces cerevisiae." Molecular and Cellular Biology 8, no. 5 (May 1988): 2184–94. http://dx.doi.org/10.1128/mcb.8.5.2184-2194.1988.

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Transcription directed into a Saccharomyces cerevisiae autonomously replicating sequence (ARS) causes high-frequency loss of minichromosomes. Conditionally stable artificial yeast chromosomes were constructed that contain an inducible GAL promoter upstream of ARS1. Under growth conditions in which the promoter was inactive, these chromosomes were mitotically stable; however, when the GAL promoter was induced, the chromosomes became extremely unstable as a result of transcriptional impairment of ARS function. This interference by the GAL promoter occurred only in cis but can occur from either side of ARS1. Transcriptional interference of ARS function can be monitored readily by using a visual colony-color assay (P. Hieter, C. Mann, M. Snyder, and R.W. Davis, Cell 40:381-392, 1985), which was further developed as a sensitive in vivo assay for sequences which rescue ARS from transcription. DNA fragments from the 3' ends of genes, inserted downstream of the GAL promoter, protected ARS function from transcriptional interference. This assay is expected to be independent of both RNA transcript stability and processing. Philippsen et al. have shown that transcription into a yeast centromere inhibits CEN function in vivo (L. Panzeri, I. Groth-Clausen, J. Shepard, A. Stotz, and P. Philippsen, Chromosomes Today 8:46-58, 1984). We identified two 200- to 300-base-pair DNA fragments flanking CEN4 that rescued ARS1 from transcription. Both of these fragments protected ARS from transcription when inserted in either orientation. The 3' ends of stable transcripts are encoded by fragments that protected the ARS from transcription, suggesting that the protection was achieved by transcription termination. It is suggested that protection of elements important for the replication and segregation of eucaryotic chromosomes from transcription is necessary for their proper function in vivo.

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Snyder, M., R. J. Sapolsky, and R. W. Davis. "Transcription interferes with elements important for chromosome maintenance in Saccharomyces cerevisiae." Molecular and Cellular Biology 8, no. 5 (May 1988): 2184–94. http://dx.doi.org/10.1128/mcb.8.5.2184.

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Transcription directed into a Saccharomyces cerevisiae autonomously replicating sequence (ARS) causes high-frequency loss of minichromosomes. Conditionally stable artificial yeast chromosomes were constructed that contain an inducible GAL promoter upstream of ARS1. Under growth conditions in which the promoter was inactive, these chromosomes were mitotically stable; however, when the GAL promoter was induced, the chromosomes became extremely unstable as a result of transcriptional impairment of ARS function. This interference by the GAL promoter occurred only in cis but can occur from either side of ARS1. Transcriptional interference of ARS function can be monitored readily by using a visual colony-color assay (P. Hieter, C. Mann, M. Snyder, and R.W. Davis, Cell 40:381-392, 1985), which was further developed as a sensitive in vivo assay for sequences which rescue ARS from transcription. DNA fragments from the 3' ends of genes, inserted downstream of the GAL promoter, protected ARS function from transcriptional interference. This assay is expected to be independent of both RNA transcript stability and processing. Philippsen et al. have shown that transcription into a yeast centromere inhibits CEN function in vivo (L. Panzeri, I. Groth-Clausen, J. Shepard, A. Stotz, and P. Philippsen, Chromosomes Today 8:46-58, 1984). We identified two 200- to 300-base-pair DNA fragments flanking CEN4 that rescued ARS1 from transcription. Both of these fragments protected ARS from transcription when inserted in either orientation. The 3' ends of stable transcripts are encoded by fragments that protected the ARS from transcription, suggesting that the protection was achieved by transcription termination. It is suggested that protection of elements important for the replication and segregation of eucaryotic chromosomes from transcription is necessary for their proper function in vivo.

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20

Tavernarakis, Nektarios, and George Thireos. "Transcriptional interference caused by GCN4 overexpression reveals multiple interactions mediating transcriptional activation." Molecular and General Genetics MGG 247, no. 5 (September 1995): 571–78. http://dx.doi.org/10.1007/bf00290348.

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Schweizer, Sophie, Christoph Harms, Heike Lerch, Jennifer Flynn, Jochen Hecht, Ferah Yildirim, Andreas Meisel, and Stefanie Märschenz. "Inhibition of Histone Methyltransferases SUV39H1 and G9a Leads to Neuroprotection in an in vitro Model of Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 35, no. 10 (May 13, 2015): 1640–47. http://dx.doi.org/10.1038/jcbfm.2015.99.

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Cerebral ischemia induces a complex transcriptional response with global changes in gene expression. It is essentially regulated by transcription factors as well as epigenetic players. While it is well known that the inhibition of transcriptionally repressive histone deacetylases leads to neuroprotection, the role of histone methyltransferases in the postischemic transcriptional response remains elusive. We investigated the effects of inhibition of the repressive H3K9 histone methyltransferases SUV39H1 and G9a on neuronal survival, H3K9 promoter signatures and gene expression. Their inhibition either with the specific blocker chaetocin or by use of RNA interference promoted neuronal survival in oxygen glucose deprivation (OGD). Brain-derived neurotrophic factor (BDNF) was upregulated and BDNF promoter regions showed an increase in histone marks characteristic for active transcription. The BDNF blockade with K252a abrogated the protective effect of chaetocin treatment. In conclusion, inhibition of histone methyltransferases SUV39H1 and G9a confers neuroprotection in a model of hypoxic metabolic stress, which is at least in part mediated by BDNF.

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Mortlock, Douglas P., Zhi-Ming Fang, Kelly J. Chandler, Yue Hou, Lissett R. Bickford, Charles E. de Bock, Valsamma Eapen, and Raymond A. Clarke. "Transcriptional Interference Regulates the Evolutionary Development of Speech." Genes 13, no. 7 (July 4, 2022): 1195. http://dx.doi.org/10.3390/genes13071195.

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The human capacity to speak is fundamental to our advanced intellectual, technological and social development. Yet so very little is known regarding the evolutionary genetics of speech or its relationship with the broader aspects of evolutionary development in primates. In this study, we describe a large family with evolutionary retrograde development of the larynx and wrist. The family presented with severe speech impairment and incremental retrograde elongations of the pisiform in the wrist that limited wrist rotation from 180° to 90° as in primitive primates. To our surprise, we found that a previously unknown primate-specific gene TOSPEAK had been disrupted in the family. TOSPEAK emerged de novo in an ancestor of extant primates across a 540 kb region of the genome with a pre-existing highly conserved long-range laryngeal enhancer for a neighbouring bone morphogenetic protein gene GDF6. We used transgenic mouse modelling to identify two additional GDF6 long-range enhancers within TOSPEAK that regulate GDF6 expression in the wrist. Disruption of TOSPEAK in the affected family blocked the transcription of TOSPEAK across the 3 GDF6 enhancers in association with a reduction in GDF6 expression and retrograde development of the larynx and wrist. Furthermore, we describe how TOSPEAK developed a human-specific promoter through the expansion of a penta-nucleotide direct repeat that first emerged de novo in the promoter of TOSPEAK in gibbon. This repeat subsequently expanded incrementally in higher hominids to form an overlapping series of Sp1/KLF transcription factor consensus binding sites in human that correlated with incremental increases in the promoter strength of TOSPEAK with human having the strongest promoter. Our research indicates a dual evolutionary role for the incremental increases in TOSPEAK transcriptional interference of GDF6 enhancers in the incremental evolutionary development of the wrist and larynx in hominids and the human capacity to speak and their retrogression with the reduction of TOSPEAK transcription in the affected family.

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Racanelli, Alexandra C., Fiona B. Turner, Lin-Ying Xie, Shirley M. Taylor, and Richard G. Moran. "A Mouse Gene That Coordinates Epigenetic Controls and Transcriptional Interference To Achieve Tissue-Specific Expression." Molecular and Cellular Biology 28, no. 2 (November 12, 2007): 836–48. http://dx.doi.org/10.1128/mcb.01088-07.

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ABSTRACT The mouse fpgs gene uses two distantly placed promoters to produce functionally distinct isozymes in a tissue-specific pattern. We queried how the P1 and P2 promoters were differentially controlled. DNA methylation of the CpG-sparse P1 promoter occurred only in tissues not initiating transcription at this site. The P2 promoter, which was embedded in a CpG island, appeared open to transcription in all tissues by several criteria, including lack of DNA methylation, yet was used only in dividing tissues. The patterns of histone modifications over the two promoters were very different: over P1, histone activation marks (acetylated histones H3 and H4 and H3 trimethylated at K4) reflected transcriptional activity and apparently reinforced the effects of hypomethylated CpGs; over P2, these marks were present in tissues whether P2 was active, inactive, or engaged in assembly of futile initiation complexes. Since P1 transcriptional activity coexisted with silencing of P2, we sought the mechanism of this transcriptional interference. We found RNA polymerase II, phosphorylated in a pattern consistent with transcriptional elongation, and only minimal levels of initiation factors over P2 in liver. We concluded that mouse fpgs uses DNA methylation to control tissue-specific expression from a CpG-sparse promoter, which is dominant over a downstream promoter masked by promoter occlusion.

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O’Connor, Nolan J., Antoni E. Bordoy, and Anushree Chatterjee. "Engineering Transcriptional Interference through RNA Polymerase Processivity Control." ACS Synthetic Biology 10, no. 4 (March 12, 2021): 737–48. http://dx.doi.org/10.1021/acssynbio.0c00534.

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Hedtke, B., and B. Grimm. "Silencing of a plant gene by transcriptional interference." Nucleic Acids Research 37, no. 11 (April 17, 2009): 3739–46. http://dx.doi.org/10.1093/nar/gkp241.

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Ghosh, Soumendu, Tripti Bameta, Dipanwita Ghanti, and Debashish Chowdhury. "A multispecies exclusion model inspired by transcriptional interference." Journal of Statistical Mechanics: Theory and Experiment 2016, no. 12 (December 23, 2016): 123501. http://dx.doi.org/10.1088/1742-5468/aa50dd.

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Palvimo, Jorma J., Piia Reinikainen, Tarja Ikonen, Pekka J. Kallio, Anu Moilanen, and Olli A. Jänne. "Mutual Transcriptional Interference between RelA and Androgen Receptor." Journal of Biological Chemistry 271, no. 39 (September 27, 1996): 24151–56. http://dx.doi.org/10.1074/jbc.271.39.24151.

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Hoffmann, Stefan A., Nan Hao, Keith E. Shearwin, and Katja M. Arndt. "Characterizing Transcriptional Interference between Converging Genes in Bacteria." ACS Synthetic Biology 8, no. 3 (February 5, 2019): 466–73. http://dx.doi.org/10.1021/acssynbio.8b00477.

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Assis, Raquel. "Transcriptional Interference Promotes Rapid Expression Divergence ofDrosophilaNested Genes." Genome Biology and Evolution 8, no. 10 (September 23, 2016): 3149–58. http://dx.doi.org/10.1093/gbe/evw237.

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Binder, Stefan, and Axel Brennicke. "Gene expression in plant mitochondria: transcriptional and post–transcriptional control." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 358, no. 1429 (January 29, 2003): 181–89. http://dx.doi.org/10.1098/rstb.2002.1179.

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The informational content of the mitochondrial genome in plants is, although small, essential for each cell. Gene expression in these organelles involves a number of distinct transcriptional and post–transcriptional steps. The complex post–transcriptional processes of plant mitochondria such as 5′ and 3′ RNA processing, intron splicing, RNA editing and controlled RNA stability extensively modify individual steady–state RNA levels and influence the mRNA quantities available for translation. In this overview of the processes in mitochondrial gene expression, we focus on confirmed and potential sites of regulatory interference and discuss the evolutionary origins of the transcriptional and post–transcriptional processes.

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Martin, B. K., and J. H. Weis. "Functional identification of transcription control sequences of the mouse Crry gene." Journal of Immunology 151, no. 2 (July 15, 1993): 857–69. http://dx.doi.org/10.4049/jimmunol.151.2.857.

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Abstract The mouse C receptor-related gene Crry is expressed by a wide variety of cells. Those sequences required for the transcriptional control of this gene were identified by deletion analysis of regions 5' of the initiating ATG. Fusion of Crry promoter sequences to the reporter gene CAT identified a region approximately 1,500 bp upstream of the transcriptional start site that enhanced transcription of this gene construct. Gel shift and methylation interference assays were performed, and a specific protein-DNA complex was identified within this region. These assays defined a 16-bp sequence 1,642 bp 5' of the initiating ATG that bound a protein in nuclear extracts prepared from all murine cell lines and tissues examined. The methylation interference assay indicated that the core region of the DNA sequence recognized by the protein was GGAA, the common core binding site for the ets family of proto-oncogenes. Oligonucleotides prepared from this sequence with the GGAA sequence did inhibit the DNA/protein complex formation, whereas those with a mutant GGAA sites did not. The minimal site identified by methylation interference was able to up-regulate transcription when placed downstream of a heterologous promoter, whereas the same sequence with an altered GGAA site could not. Thus, this site functions as an enhancer.

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Wang, Kai, Feng Sun, and Hui Z. Sheng. "Regulated expression of TAF1 in 1-cell mouse embryos." Zygote 14, no. 3 (August 2006): 209–15. http://dx.doi.org/10.1017/s0967199406003704.

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SummaryTATA binding protein (TBP) associated factor 1 (TAF1) is a member of the general transcription machinery. Interference in the function of TAF1 causes a broad transcriptional defect in early development. To explore possible roles of TAF1 in embryonic transcriptional silence and zygotic genome activation, we examined the expression of TAF1 in 1-cell mouse embryos. Using an immunofluorescence assay, TAF1 was not detected in embryos in the first few hours after fertilization. TAF1 appeared in pronuclei 6 h post-fertilization and reached a relatively high level before zygotic genome activation. These data show that besides TBP, another critical member of the general transcription machinery such as TAF1 is also absent or at an extremely low level at the outset of development. Combined deficiency in critical members of the general transcription machinery may account for embryonic transcriptional silence.

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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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Kannan, Perry, and Michael A. Tainsky. "Coactivator PC4 Mediates AP-2 Transcriptional Activity and Suppresses ras-Induced Transformation Dependent on AP-2 Transcriptional Interference." Molecular and Cellular Biology 19, no. 1 (January 1, 1999): 899–908. http://dx.doi.org/10.1128/mcb.19.1.899.

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ABSTRACT ras oncogene-transformed PA-1 human teratocarcinoma cells have abundant AP-2 mRNA but, paradoxically, little AP-2 transcriptional activity. We have previously shown that overexpression of AP-2 in nontumorigenic variants of PA-1 cells results in inhibition of AP-2 activity and induction of tumorigenicity similar to that caused by ras transformation of PA-1 cells. Evidence indicated the existence of a novel mechanism of inhibition of AP-2 activity involving sequestering of transcriptional coactivators. In this study, we found that PC4 is a positive coactivator of AP-2 and can restore AP-2 activity in ras-transformed PA-1 cells. Relative to vector-transfected ras cell lines,ras cell lines stably transfected with and expressing the PC4 cDNA have a diminished growth rate and exhibit a loss of anchorage-independent growth, and they are unable to induce the formation of tumors in nude mice. These data suggest that a transcriptional coactivator, like a tumor suppressor, can have a growth-suppressive effect on cells. Our experiments are the first to show that ras oncogenes and oncogenic transcription factors can induce transformation through effects on the transcription machinery rather than through specific programs of gene expression.

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Assis, Raquel. "No Expression Divergence despite Transcriptional Interference between Nested Protein-Coding Genes in Mammals." Genes 12, no. 9 (September 1, 2021): 1381. http://dx.doi.org/10.3390/genes12091381.

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Nested protein-coding genes accumulated throughout metazoan evolution, with early analyses of human and Drosophila microarray data indicating that this phenomenon was simply due to the presence of large introns. However, a recent study employing RNA-seq data uncovered evidence of transcriptional interference driving rapid expression divergence between Drosophila nested genes, illustrating that accurate expression estimation of overlapping genes can enhance detection of their relationships. Hence, here I apply an analogous approach to strand-specific RNA-seq data from human and mouse to revisit the role of transcriptional interference in the evolution of mammalian nested genes. A genomic survey reveals that whereas mammalian nested genes indeed accrued over evolutionary time, they are retained at lower frequencies than in Drosophila. Though several properties of mammalian nested genes align with observations in Drosophila and with expectations under transcriptional interference, contrary to both, their expression divergence is not statistically different from that between unnested genes, and also does not increase after nesting. Together, these results support the hypothesis that lower selection efficiencies limit rates of gene expression evolution in mammals, leading to their reliance on immediate eradication of deleterious nested genes to avoid transcriptional interference.

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Soddu, S., G. Blandino, R. Scardigli, S. Coen, A. Marchetti, M. G. Rizzo, G. Bossi, L. Cimino, M. Crescenzi, and A. Sacchi. "Interference with p53 protein inhibits hematopoietic and muscle differentiation." Journal of Cell Biology 134, no. 1 (July 1, 1996): 193–204. http://dx.doi.org/10.1083/jcb.134.1.193.

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The involvement of p53 protein in cell differentiation has been recently suggested by some observations made with tumor cells and the correlation found between differentiation and increased levels of p53. However, the effect of p53 on differentiation is in apparent contrast with the normal development of p53-null mice. To test directly whether p53 has a function in cell differentiation, we interfered with the endogenous wt-p53 protein of nontransformed cells of two different murine histotypes: 32D myeloid progenitors, and C2C12 myoblasts. A drastic inhibition of terminal differentiation into granulocytes or myotubes, respectively, was observed upon expression of dominant-negative p53 proteins. This inhibition did not alter the cell cycle withdrawal typical of terminal differentiation, nor p21(WAF1/CIP1) upregulation, indicating that interference with endogenous p53 directly affects cell differentiation, independently of the p53 activity on the cell cycle. We also found that the endogenous wt-p53 protein of C2C12 cells becomes transcriptionally active during myogenesis, and this activity is inhibited by p53 dominant-negative expression. Moreover, we found that p53 DNA-binding and transcriptional activities are both required to induce differentiation in p53-negative K562 cells. Taken together, these data strongly indicate that p53 is a regulator of cell differentiation and it exerts this role, at least in part, through its transcriptional activity.

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Sidahmed, Abubaker, Shaza Abdalla, Salahedin Mahmud, and Bruce Wilkie. "Antiviral innate immune response of RNA interference." Journal of Infection in Developing Countries 8, no. 07 (July 14, 2014): 804–10. http://dx.doi.org/10.3855/jidc.4187.

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RNA interference (RNAi) is an ancient, natural process conserved among species from different kingdoms. RNAi is a transcriptional and post-transcriptional gene silencing mechanism in which, double-stranded RNA or hairpin RNA is cleaved by an RNase III-type enzyme called Dicer into small interfering RNA duplex. This subsequently directs sequence-specific, homology dependent, Watson-Crick base-pairing post-transcriptional gene silencing by binding to its complementary RNA and initiating its elimination through degradation or by persuading translational inhibition. In plants, worms, and insects, RNAi is the main and strong antiviral defense mechanism. It is clear that RNAi silencing, contributes in restriction of viral infection in vertebrates. In a short period, RNAi has progressed to become a significant experimental tool for the analysis of gene function and target validation in mammalian systems. In addition, RNA silencing has then been found to be involved in translational repression, transcriptional inhibition, and DNA degradation. RNAi machinery required for robust RNAi-mediated antiviral response are conserved throughout evolution in mammals and plays a crucial role in antiviral defense of invertebrates, but despite these important functions RNAi contribution to mammalian antiviral innate immune defense has been underestimated and disputed. In this article, we review the literature concerning the roles of RNAi as components of innate immune system in mammals and how, the RNAi is currently one of the most hopeful new advances toward disease therapy. This review highlights the potential of RNAi as a therapeutic strategy for viral infection and gene regulation to modulate host immune response to viral infection.

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Korde, Asawari, Jessica M. Rosselot, and David Donze. "Intergenic Transcriptional Interference Is Blocked by RNA Polymerase III Transcription Factor TFIIIB inSaccharomyces cerevisiae." Genetics 196, no. 2 (December 13, 2013): 427–38. http://dx.doi.org/10.1534/genetics.113.160093.

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Knutson, Bruce A., Jaewook Oh, and Steven S. Broyles. "Downregulation of vaccinia virus intermediate and late promoters by host transcription factor YY1." Journal of General Virology 90, no. 7 (July 1, 2009): 1592–99. http://dx.doi.org/10.1099/vir.0.006924-0.

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Approximately half of the intermediate and late gene transcriptional promoters of vaccinia virus have a binding site for the cellular transcription factor YY1 that overlaps the initiator elements. Depletion of YY1 using RNA interference enhanced the activity of these promoters, while overexpression of YY1 repressed their activity. Viral promoter nucleotide replacements that specifically impair the binding of YY1 mostly alleviated the transcriptional repression and correlated with the ability of YY1 to stably interact with the initiator DNAs in vitro. The transcriptional repression activity was localized to the C-terminal DNA-binding domain of the protein. These results indicate that YY1 functions to negatively regulate these vaccinia virus promoters by binding to their initiator elements.

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Noma, Ken-ichi, Tomoyasu Sugiyama, Hugh Cam, Andre Verdel, Martin Zofall, Songtao Jia, Danesh Moazed, and Shiv I. S. Grewal. "RITS acts in cis to promote RNA interference–mediated transcriptional and post-transcriptional silencing." Nature Genetics 36, no. 11 (October 10, 2004): 1174–80. http://dx.doi.org/10.1038/ng1452.

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Baker, Christopher R., Victor Hanson-Smith, and Alexander D. Johnson. "Following Gene Duplication, Paralog Interference Constrains Transcriptional Circuit Evolution." Science 342, no. 6154 (October 3, 2013): 104–8. http://dx.doi.org/10.1126/science.1240810.

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Most models of gene duplication assume that the ancestral functions of the preduplication gene are independent and can therefore be neatly partitioned between descendant paralogs. However, many gene products, such as transcriptional regulators, are components within cooperative assemblies; here, we show that a natural consequence of duplication and divergence of such proteins can be competitive interference between the paralogs. Our example is based on the duplication of the essential MADS-box transcriptional regulator Mcm1, which is found in all fungi and regulates a large set of genes. We show that a set of historical amino acid sequence substitutions minimized paralog interference in contemporary species and, in doing so, increased the molecular complexity of this gene regulatory network. We propose that paralog interference is a common constraint on gene duplicate evolution, and its resolution, which can generate additional regulatory complexity, is needed to stabilize duplicated genes in the genome.

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Pande, Amit, Jürgen Brosius, Izabela Makalowska, Wojciech Makalowski, and Carsten A. Raabe. "Transcriptional interference by small transcripts in proximal promoter regions." Nucleic Acids Research 46, no. 3 (January 4, 2018): 1069–88. http://dx.doi.org/10.1093/nar/gkx1242.

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Bordoy, Antoni E., Nolan J. O’Connor, and Anushree Chatterjee. "Construction of Two-Input Logic Gates Using Transcriptional Interference." ACS Synthetic Biology 8, no. 10 (September 18, 2019): 2428–41. http://dx.doi.org/10.1021/acssynbio.9b00321.

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Anhezini, Lucas, Ana P. Saita, Ricardo G. Ramos, and Claudio R. Simon. "Transcriptional silencing of jazigo using in vivo RNA interference." Developmental Biology 344, no. 1 (August 2010): 529. http://dx.doi.org/10.1016/j.ydbio.2010.05.388.

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Dodd, Ian B., Keith E. Shearwin, and Kim Sneppen. "Modelling Transcriptional Interference and DNA Looping in Gene Regulation." Journal of Molecular Biology 369, no. 5 (June 2007): 1200–1213. http://dx.doi.org/10.1016/j.jmb.2007.04.041.

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Karkare, Shantanu, Saurabha Daniel, and Deepak Bhatnagar. "RNA Interference Silencing the Transcriptional Message: Aspects and Applications." Applied Biochemistry and Biotechnology 119, no. 1 (2004): 01–12. http://dx.doi.org/10.1385/abab:119:1:01.

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Valerius, Oliver, Cornelia Brendel, Katrin Düvel, and Gerhard H. Braus. "Multiple Factors Prevent Transcriptional Interference at the YeastARO4-HIS7Locus." Journal of Biological Chemistry 277, no. 24 (April 5, 2002): 21440–45. http://dx.doi.org/10.1074/jbc.m201841200.

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Na, K. Y. "Silencing of TonEBP/NFAT5 Transcriptional Activator by RNA Interference." Journal of the American Society of Nephrology 14, no. 2 (February 1, 2003): 283–88. http://dx.doi.org/10.1097/01.asn.0000045050.19544.b2.

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Colgin, Mark A., and Jennifer K. Nyborg. "The Human T-Cell Leukemia Virus Type 1 Oncoprotein Tax Inhibits the Transcriptional Activity of c-Myb through Competition for the CREB Binding Protein." Journal of Virology 72, no. 11 (November 1, 1998): 9396–99. http://dx.doi.org/10.1128/jvi.72.11.9396-9399.1998.

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ABSTRACT Tax, the transforming protein of human T-cell leukemia virus type 1 (HTLV-1), is required for strong activation of HTLV-1 transcription. This activation is mediated through interaction with the KIX domain of the cellular coactivator CREB binding protein (CBP). In this study we examined the possibility that the Tax-KIX interaction may mediate effects on cellular gene transcription in vivo, as a growing number of cellular transcription factors have been shown to utilize CBP as a coactivator. We tested the ability of Tax to deregulate the activity of the cellular transcription factor, c-Myb, since both Tax and c-Myb interact with the KIX domain of CBP. Our results show that in vivo, Tax antagonizes the transcriptional activity of c-Myb and, reciprocally, c-Myb antagonizes the transcriptional activity of Tax. Furthermore, c-Myb competes for KIX binding to Tax in vitro, indicating that these two transcription factors bind CBP in a mutually exclusive manner. This novel mechanism of transcriptional interference by Tax may promote globally deregulated cellular gene expression in the HTLV-1-infected cell, possibly leading to leukemogenesis.

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Castro Alvarez, Javier J., Maxime Revel, Judit Carrasco, Fabienne Cléard, Daniel Pauli, Valérie Hilgers, François Karch, and Robert K. Maeda. "Repression of the Hox gene abd-A by ELAV-mediated Transcriptional Interference." PLOS Genetics 17, no. 11 (November 15, 2021): e1009843. http://dx.doi.org/10.1371/journal.pgen.1009843.

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Intergenic transcription is a common feature of eukaryotic genomes and performs important and diverse cellular functions. Here, we investigate the iab-8 ncRNA from the Drosophila Bithorax Complex and show that this RNA is able to repress the transcription of genes located at its 3’ end by a sequence-independent, transcriptional interference mechanism. Although this RNA is expressed in the early epidermis and CNS, we find that its repressive activity is limited to the CNS, where, in wild-type embryos, it acts on the Hox gene, abd-A, located immediately downstream of it. The CNS specificity is achieved through a 3’ extension of the transcript, mediated by the neuronal-specific, RNA-binding protein, ELAV. Loss of ELAV activity eliminates the 3’ extension and results in the ectopic activation of abd-A. Thus, a tissue-specific change in the length of a ncRNA is used to generate a precise pattern of gene expression in a higher eukaryote.

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Journal articles on the topic 'Transcriptional interference'

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