Journal articles: 'Transcription mechanism'

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Sui, Zhiyuan, Yongjie Zhang, Zhishuai Zhang, Chenguang Wang, Xiaojun Li, Feng Xing, and Mingxing Chu. "Analysis of Lin28B Promoter Activity and Screening of Related Transcription Factors in Dolang Sheep." Genes 14, no. 5 (May 7, 2023): 1049. http://dx.doi.org/10.3390/genes14051049.

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The Lin28B gene is involved in the initiation of puberty, but its regulatory mechanisms remain unclear. Therefore, in this study, we aimed to study the regulatory mechanism of the Lin28B promoter by cloning the Lin28B proximal promoter for bioinformatic analysis. Next, a series of deletion vectors were constructed based on the bioinformatic analysis results for dual-fluorescein activity detection. The transcriptional regulation mechanism of the Lin28B promoter region was analyzed by detecting mutations in transcription factor-binding sites and overexpression of transcription factors. The dual-luciferase assay showed that the Lin28B promoter region −837 to −338 bp had the highest transcriptional activity, and the transcriptional activity of the Lin28B transcriptional regulatory region decreased significantly after Egr1 and SP1 mutations. Overexpression of the Egr1 transcription factor significantly enhanced the transcription of Lin28B, and the results indicated that Egr1 and SP1 play important roles in regulating Lin28B. These results provide a theoretical basis for further research on the transcriptional regulation of sheep Lin28B during puberty initiation.

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HANDA, HIROSHI. "Mechanism of adenovirus transcription." Uirusu 37, no. 2 (1987): 229–40. http://dx.doi.org/10.2222/jsv.37.229.

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Basu, Urmimala, Alicia M. Bostwick, Kalyan Das, Kristin E. Dittenhafer-Reed, and Smita S. Patel. "Structure, mechanism, and regulation of mitochondrial DNA transcription initiation." Journal of Biological Chemistry 295, no. 52 (October 30, 2020): 18406–25. http://dx.doi.org/10.1074/jbc.rev120.011202.

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Mitochondria are specialized compartments that produce requisite ATP to fuel cellular functions and serve as centers of metabolite processing, cellular signaling, and apoptosis. To accomplish these roles, mitochondria rely on the genetic information in their small genome (mitochondrial DNA) and the nucleus. A growing appreciation for mitochondria's role in a myriad of human diseases, including inherited genetic disorders, degenerative diseases, inflammation, and cancer, has fueled the study of biochemical mechanisms that control mitochondrial function. The mitochondrial transcriptional machinery is different from nuclear machinery. The in vitro re-constituted transcriptional complexes of Saccharomyces cerevisiae (yeast) and humans, aided with high-resolution structures and biochemical characterizations, have provided a deeper understanding of the mechanism and regulation of mitochondrial DNA transcription. In this review, we will discuss recent advances in the structure and mechanism of mitochondrial transcription initiation. We will follow up with recent discoveries and formative findings regarding the regulatory events that control mitochondrial DNA transcription, focusing on those involved in cross-talk between the mitochondria and nucleus.

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Xu, Jun, Jenny Chong, and Dong Wang. "Strand-specific effect of Rad26 and TFIIS in rescuing transcriptional arrest by CAG trinucleotide repeat slip-outs." Nucleic Acids Research 49, no. 13 (July 1, 2021): 7618–27. http://dx.doi.org/10.1093/nar/gkab573.

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Abstract Transcription induced CAG repeat instability is associated with fatal neurological disorders. Genetic approaches found transcription-coupled nucleotide excision repair (TC-NER) factor CSB protein and TFIIS play critical roles in modulating the repeat stability. Here, we took advantage of an in vitro reconstituted yeast transcription system to investigate the underlying mechanism of RNA polymerase II (Pol II) transcriptional pausing/stalling by CAG slip-out structures and the functions of TFIIS and Rad26, the yeast ortholog of CSB, in modulating transcriptional arrest. We identified length-dependent and strand-specific mechanisms that account for CAG slip-out induced transcriptional arrest. We found substantial R-loop formation for the distal transcriptional pausing induced by template strand (TS) slip-out, but not non-template strand (NTS) slip-out. In contrast, Pol II backtracking was observed at the proximal transcriptional pausing sites induced by both NTS and TS slip-out blockage. Strikingly, we revealed that Rad26 and TFIIS can stimulate bypass of NTS CAG slip-out, but not TS slip-out induced distal pausing. Our biochemical results provide new insights into understanding the mechanism of CAG slip-out induced transcriptional pausing and functions of transcription factors in modulating transcription-coupled CAG repeat instability, which may pave the way for developing potential strategies for the treatment of repeat sequence associated human diseases.

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Wang, Yaolai, Jiaming Qi, Jie Shao, and Xu-Qing Tang. "Signaling Mechanism of Transcriptional Bursting: A Technical Resolution-Independent Study." Biology 9, no. 10 (October 19, 2020): 339. http://dx.doi.org/10.3390/biology9100339.

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Gene transcription has been uncovered to occur in sporadic bursts. However, due to technical difficulties in differentiating individual transcription initiation events, it remains debated as to whether the burst size, frequency, or both are subject to modulation by transcriptional activators. Here, to bypass technical constraints, we addressed this issue by introducing two independent theoretical methods including analytical research based on the classic two-model and information entropy research based on the architecture of transcription apparatus. Both methods connect the signaling mechanism of transcriptional bursting to the characteristics of transcriptional uncertainty (i.e., the differences in transcriptional levels of the same genes that are equally activated). By comparing the theoretical predictions with abundant experimental data collected from published papers, the results exclusively support frequency modulation. To further validate this conclusion, we showed that the data that appeared to support size modulation essentially supported frequency modulation taking into account the existence of burst clusters. This work provides a unified scheme that reconciles the debate on burst signaling.

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Lopez, Alex B., Chuanping Wang, Charlie C. Huang, Ibrahim Yaman, Yi Li, Kaushik Chakravarty, Peter F. Johnson, et al. "A feedback transcriptional mechanism controls the level of the arginine/lysine transporter cat-1 during amino acid starvation." Biochemical Journal 402, no. 1 (January 25, 2007): 163–73. http://dx.doi.org/10.1042/bj20060941.

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The adaptive response to amino acid limitation in mammalian cells inhibits global protein synthesis and promotes the expression of proteins that protect cells from stress. The arginine/lysine transporter, cat-1, is induced during amino acid starvation by transcriptional and post-transcriptional mechanisms. It is shown in the present study that the transient induction of cat-1 transcription is regulated by the stress response pathway that involves phosphorylation of the translation initiation factor, eIF2 (eukaryotic initiation factor-2). This phosphorylation induces expression of the bZIP (basic leucine zipper protein) transcription factors C/EBP (CCAAT/enhancer-binding protein)-β and ATF (activating transcription factor) 4, which in turn induces ATF3. Transfection experiments in control and mutant cells, and chromatin immunoprecipitations showed that ATF4 activates, whereas ATF3 represses cat-1 transcription, via an AARE (amino acid response element), TGATGAAAC, in the first exon of the cat-1 gene, which functions both in the endogenous and in a heterologous promoter. ATF4 and C/EBPβ activated transcription when expressed in transfected cells and they bound as heterodimers to the AARE in vitro. The induction of transcription by ATF4 was inhibited by ATF3, which also bound to the AARE as a heterodimer with C/EBPβ. These results suggest that the transient increase in cat-1 transcription is due to transcriptional activation caused by ATF4 followed by transcriptional repression by ATF3 via a feedback mechanism.

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Medina, Gerardo, Katy Juárez, Brenda Valderrama, and Gloria Soberón-Chávez. "Mechanism of Pseudomonas aeruginosa RhlR Transcriptional Regulation of the rhlAB Promoter." Journal of Bacteriology 185, no. 20 (October 15, 2003): 5976–83. http://dx.doi.org/10.1128/jb.185.20.5976-5983.2003.

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ABSTRACT Pseudomonas aeruginosa contains two transcription regulators (LasR and RhlR) that, when complexed with their specific autoinducers (3-oxo-dodecanoyl-homoserine lactone and butanoyl-homoserine lactone, respectively) activate transcription of different virulence-associated traits. We studied the RhlR-dependent transcriptional regulation of the rhlAB operon encoding rhamnosyltransferase 1, an enzyme involved in the synthesis of the surfactant monorhamnolipid, and showed that RhlR binds to a specific sequence in the rhlAB regulatory region, both in the presence and in the absence of its autoinducer. Our data suggest that in the former case it activates transcription, whereas in the latter it acts as a transcriptional repressor of this promoter. RhlR seems to repress the transcription of other quorum-sensing-regulated genes; thus, RhlR repressor activity might be of importance in the finely regulated expression of P. aeruginosa virulence-associated traits.

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Jackson, Kelly A., Ruth A. Valentine, Lisa J. Coneyworth, John C. Mathers, and Dianne Ford. "Mechanisms of mammalian zinc-regulated gene expression." Biochemical Society Transactions 36, no. 6 (November 19, 2008): 1262–66. http://dx.doi.org/10.1042/bst0361262.

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Mechanisms through which gene expression is regulated by zinc are central to cellular zinc homoeostasis. In this context, evidence for the involvement of zinc dyshomoeostasis in the aetiology of diseases, including Type 2 diabetes, Alzheimer's disease and cancer, highlights the importance of zinc-regulated gene expression. Mechanisms elucidated in bacteria and yeast provide examples of different possible modes of zinc-sensitive gene regulation, involving the zinc-regulated binding of transcriptional activators and repressors to gene promoter regions. A mammalian transcriptional regulatory mechanism that mediates zinc-induced transcriptional up-regulation, involving the transcription factor MTF1 (metal-response element-binding transcription factor 1), has been studied extensively. Gene responses in the opposite direction (reduced mRNA levels in response to increased zinc availability) have been observed in mammalian cells, but a specific transcriptional regulatory process responsible for such a response has yet to be identified. Examples of single zinc-sensitive transcription factors regulating gene expression in opposite directions are emerging. Although zinc-induced transcriptional repression by MTF1 is a possible explanation in some specific instances, such a mechanism cannot account for repression by zinc of all mammalian genes that show this mode of regulation, indicating the existence of as yet uncharacterized mechanisms of zinc-regulated transcription in mammalian cells. In addition, recent findings reveal a role for effects of zinc on mRNA stability in the regulation of specific zinc transporters. Our studies on the regulation of the human gene SLC30A5 (solute carrier 30A5), which codes for the zinc transporter ZnT5, have revealed that this gene provides a model system by which to study both zinc-induced transcriptional down-regulation and zinc-regulated mRNA stabilization.

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Lee, Sang C., Angeliki Magklara, and Catharine L. Smith. "HDAC Activity Is Required for Efficient Core Promoter Function at the Mouse Mammary Tumor Virus Promoter." Journal of Biomedicine and Biotechnology 2011 (2011): 1–14. http://dx.doi.org/10.1155/2011/416905.

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Histone deacetylases (HDACs) have been shown to be required for basal or inducible transcription at a variety of genes by poorly understood mechanisms. We demonstrated previously that HDAC inhibition rapidly repressed transcription from the mouse mammary tumor virus (MMTV) promoter by a mechanism that does not require the binding of upstream transcription factors. In the current study, we find that HDACs work through the core promoter sequences of MMTV as well as those of several cellular genes to facilitate transcriptional initiation through deacetylation of nonhistone proteins.

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Nudler, E., A. Goldfarb, and M. Kashlev. "Discontinuous mechanism of transcription elongation." Science 265, no. 5173 (August 5, 1994): 793–96. http://dx.doi.org/10.1126/science.8047884.

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Yuzenkova, Yulia, Aleksandra Bochkareva, Vasisht R. Tadigotla, Mohammad Roghanian, Savva Zorov, Konstantin Severinov, and Nikolay Zenkin. "Stepwise mechanism for transcription fidelity." BMC Biology 8, no. 1 (2010): 54. http://dx.doi.org/10.1186/1741-7007-8-54.

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12

Haidara, Nouhou, Marta Giannini, and Odil Porrua. "Modulated termination of non-coding transcription partakes in the regulation of gene expression." Nucleic Acids Research 50, no. 3 (January 17, 2022): 1430–48. http://dx.doi.org/10.1093/nar/gkab1304.

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Abstract Pervasive transcription is a universal phenomenon leading to the production of a plethora of non-coding RNAs. If left uncontrolled, pervasive transcription can be harmful for genome expression and stability. However, non-coding transcription can also play important regulatory roles, for instance by promoting the repression of specific genes by a mechanism of transcriptional interference. The efficiency of transcription termination can strongly influence the regulatory capacity of non-coding transcription events, yet very little is known about the mechanisms modulating the termination of non-coding transcription in response to environmental cues. Here, we address this question by investigating the mechanisms that regulate the activity of the main actor in termination of non-coding transcription in budding yeast, the helicase Sen1. We identify a phosphorylation at a conserved threonine of the catalytic domain of Sen1 and we provide evidence that phosphorylation at this site reduces the efficiency of Sen1-mediated termination. Interestingly, we find that this phosphorylation impairs termination at an unannotated non-coding gene, thus repressing the expression of a downstream gene encoding the master regulator of Zn homeostasis, Zap1. Consequently, many additional genes exhibit an expression pattern mimicking conditions of Zn excess, where ZAP1 is naturally repressed. Our findings provide a novel paradigm of gene regulatory mechanism relying on the direct modulation of non-coding transcription termination.

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Pérez-Schindler, Joaquín, Bastian Kohl, Konstantin Schneider-Heieck, Aurel B. Leuchtmann, Carlos Henríquez-Olguín, Volkan Adak, Geraldine Maier, et al. "RNA-bound PGC-1α controls gene expression in liquid-like nuclear condensates." Proceedings of the National Academy of Sciences 118, no. 36 (August 31, 2021): e2105951118. http://dx.doi.org/10.1073/pnas.2105951118.

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Plasticity of cells, tissues, and organs is controlled by the coordinated transcription of biological programs. However, the mechanisms orchestrating such context-specific transcriptional networks mediated by the dynamic interplay of transcription factors and coregulators are poorly understood. The peroxisome proliferator–activated receptor γ coactivator 1α (PGC-1α) is a prototypical master regulator of adaptive transcription in various cell types. We now uncovered a central function of the C-terminal domain of PGC-1α to bind RNAs and assemble multiprotein complexes including proteins that control gene transcription and RNA processing. These interactions are important for PGC-1α recruitment to chromatin in transcriptionally active liquid-like nuclear condensates. Notably, such a compartmentalization of active transcription mediated by liquid–liquid phase separation was observed in mouse and human skeletal muscle, revealing a mechanism by which PGC-1α regulates complex transcriptional networks. These findings provide a broad conceptual framework for context-dependent transcriptional control of phenotypic adaptations in metabolically active tissues.

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PEI, Lin. "Transcriptional repressor of vasoactive intestinal peptide receptor mediates repression through interactions with TFIIB and TFIIEβ." Biochemical Journal 360, no. 3 (December 10, 2001): 633–38. http://dx.doi.org/10.1042/bj3600633.

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The transcriptional repressor for rat vasoactive-intestinal-polypeptide receptor 1 (VIPR-RP) is a recently characterized transcription factor that belongs to a family of proteins, which include components of the DNA replication factor C complex. In this study, I investigated the mechanisms by which VIPR-RP represses transcription. I show here that transcriptional repression by VIPR-RP is mediated by a histone deacetylase-independent mechanism. I provide evidence that VIPR-RP makes direct physical contacts with two proteins of the basal transcription apparatus, the transcription factors TFIIB and TFIIEβ. The interaction with TFIIB is mediated by the N-terminal 180 amino acids, whereas the interactive domain with TFIIEβ is located between residues 367 and 527 of VIPR-RP. Using gel mobility-shift assays I demonstrated that interaction between VIPR-RP and TFIIB prevents the recruitment of TFIIB into a DNA–TATA-box-binding protein complex. My results indicate that VIPR-RP mediates transcriptional repression through direct interactions with the general transcription machinery.

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Li, Chenlei, Zhe Zhang, Yilin Wei, Kunlong Qi, Yaqing Dou, Chenglei Song, Yingke Liu, et al. "Genome-Wide Analysis of MAMSTR Transcription Factor-Binding Sites via ChIP-Seq in Porcine Skeletal Muscle Fibroblasts." Animals 13, no. 11 (May 23, 2023): 1731. http://dx.doi.org/10.3390/ani13111731.

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Myocyte enhancer factor-2-activating motif and SAP domain-containing transcriptional regulator (MAMSTR) regulates its downstream through binding in its promoter regions. However, its molecular mechanism, particularly the DNA-binding sites, and coregulatory genes are quite unexplored. Therefore, to identify the genome-wide binding sites of the MAMSTR transcription factors and their coregulatory genes, chromatin immunoprecipitation sequencing was carried out. The results showed that MAMSTR was associated with 1506 peaks, which were annotated as 962 different genes. Most of these genes were involved in transcriptional regulation, metabolic pathways, and cell development and differentiation, such as AMPK signaling pathway, TGF-beta signaling pathway, transcription coactivator activity, transcription coactivator binding, adipocytokine signaling pathway, fat digestion and absorption, skeletal muscle fiber development, and skeletal muscle cell differentiation. Lastly, the expression levels and transcriptional activities of PID1, VTI1B, PRKAG1, ACSS2, and SLC28A3 were screened and verified via functional markers and analysis. Overall, this study has increased our understanding of the regulatory mechanism of MAMSTR during skeletal muscle fibroblast development and provided a reference for analyzing muscle development mechanisms.

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Voit, R., K. Schäfer, and I. Grummt. "Mechanism of repression of RNA polymerase I transcription by the retinoblastoma protein." Molecular and Cellular Biology 17, no. 8 (August 1997): 4230–37. http://dx.doi.org/10.1128/mcb.17.8.4230.

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The retinoblastoma susceptibility gene product pRb restricts cellular proliferation by affecting gene expression by all three classes of nuclear RNA polymerases. To elucidate the molecular mechanisms underlying pRb-mediated repression of ribosomal DNA (rDNA) transcription by RNA polymerase I, we have analyzed the effect of pRb in a reconstituted transcription system. We demonstrate that pRb, but not the related protein p107, acts as a transcriptional repressor by interfering with the assembly of transcription initiation complexes. The HMG box-containing transcription factor UBF is the main target for pRb-induced transcriptional repression. UBF and pRb form in vitro complexes involving the C-terminal part of pRb and HMG boxes 1 and 2 of UBF. We show that the interactions between UBF and TIF-IB and between UBF and RNA polymerase I, respectively, are not perturbed by pRb. However, the DNA binding activity of UBF to both synthetic cruciform DNA and the rDNA promoter is severely impaired in the presence of pRb. These studies reveal another mechanism by which pRb suppresses cell proliferation, namely, by direct inhibition of cellular rRNA synthesis.

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Landick, R. "The regulatory roles and mechanism of transcriptional pausing." Biochemical Society Transactions 34, no. 6 (October 25, 2006): 1062–66. http://dx.doi.org/10.1042/bst0341062.

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The multisubunit RNAPs (RNA polymerases) found in all cellular life forms are remarkably conserved in fundamental structure, in mechanism and in their susceptibility to sequence-dependent pausing during transcription of DNA in the absence of elongation regulators. Recent studies of both prokaryotic and eukaryotic transcription have yielded an increasing appreciation of the extent to which gene regulation is accomplished during the elongation phase of transcription. Transcriptional pausing is a fundamental enzymatic mechanism that underlies many of these regulatory schemes. In some cases, pausing functions by halting RNAP for times or at positions required for regulatory interactions. In other cases, pauses function by making RNAP susceptible to premature termination of transcription unless the enzyme is modified by elongation regulators that programme efficient gene expression. Pausing appears to occur by a two-tiered mechanism in which an initial rearrangement of the enzyme's active site interrupts active elongation and puts RNAP in an elemental pause state from which additional rearrangements or regulator interactions can create long-lived pauses. Recent findings from biochemical and single-molecule transcription experiments, coupled with the invaluable availability of RNAP crystal structures, have produced attractive hypotheses to explain the fundamental mechanism of pausing.

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Tsai, Albert, Rafael Galupa, and Justin Crocker. "Robust and efficient gene regulation through localized nuclear microenvironments." Development 147, no. 19 (October 5, 2020): dev161430. http://dx.doi.org/10.1242/dev.161430.

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ABSTRACTDevelopmental enhancers drive gene expression in specific cell types during animal development. They integrate signals from many different sources mediated through the binding of transcription factors, producing specific responses in gene expression. Transcription factors often bind low-affinity sequences for only short durations. How brief, low-affinity interactions drive efficient transcription and robust gene expression is a central question in developmental biology. Localized high concentrations of transcription factors have been suggested as a possible mechanism by which to use these enhancer sites effectively. Here, we discuss the evidence for such transcriptional microenvironments, mechanisms for their formation and the biological consequences of such sub-nuclear compartmentalization for developmental decisions and evolution.

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Yesudhas, Dhanusha, Muhammad Ayaz Anwar, and Sangdun Choi. "Structural mechanism of DNA-mediated Nanog–Sox2 cooperative interaction." RSC Advances 9, no. 14 (2019): 8121–30. http://dx.doi.org/10.1039/c8ra10085c.

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Asada, Ryuta, Naomichi Takemata, Charles S. Hoffman, Kunihiro Ohta, and Kouji Hirota. "Antagonistic Controls of Chromatin and mRNA Start Site Selection by Tup Family Corepressors and the CCAAT-Binding Factor." Molecular and Cellular Biology 35, no. 5 (December 22, 2014): 847–55. http://dx.doi.org/10.1128/mcb.00924-14.

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The Tup family corepressors contribute to critical cellular responses, such as the stress response and differentiation, presumably by inducing repressive chromatin, though the precise repression mechanism remains to be elucidated. TheSchizosaccharomyces pombefission yeast Tup family corepressors Tup11 and Tup12 (Tup11/12), which are orthologs of Tup1 inSaccharomyces cerevisiaebudding yeast and Groucho inDrosophila, negatively control chromatin and the transcriptional activity of some stress-responsive genes. Here, we demonstrate that Tup11/12 repress transcription of a gluconeogenesis gene,fbp1+, by three distinct mechanisms. First, Tup11/12 inhibit chromatin remodeling in thefbp1+promoter region where the Atf1 and Rst2 transcriptional activators bind. Second, they repress the formation of an open chromatin configuration at thefbp1+TATA box. Third, they repress mRNA transcriptionper seby regulating basic transcription factors. These inhibitory actions of Tup11/12 are antagonized by three different types of transcriptional activators: CREB/ATF-type Atf1, C2H2zinc finger-type Rst2, and CBF/NF-Y-type Php5 proteins. We also found that impaired chromatin remodeling andfbp1+mRNA transcription inphp5Δ strains are rescued by the double deletions oftup11+andtup12+, although the distribution of the transcription start sites becomes broader than that in wild-type cells. These data reveal a new mechanism of precise determination of the mRNA start site by Tup family corepressors and CBF/NF-Y proteins.

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Hokello, Joseph, Adhikarimayum Lakhikumar Sharma, and Mudit Tyagi. "Efficient Non-Epigenetic Activation of HIV Latency through the T-Cell Receptor Signalosome." Viruses 12, no. 8 (August 8, 2020): 868. http://dx.doi.org/10.3390/v12080868.

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Human immunodeficiency virus type-1 (HIV-1) can either undergo a lytic pathway to cause productive systemic infections or enter a latent state in which the integrated provirus remains transcriptionally silent for decades. The ability to latently infect T-cells enables HIV-1 to establish persistent infections in resting memory CD4+ T-lymphocytes which become reactivated following the disruption or cessation of intensive drug therapy. The maintenance of viral latency occurs through epigenetic and non-epigenetic mechanisms. Epigenetic mechanisms of HIV latency regulation involve the deacetylation and methylation of histone proteins within nucleosome 1 (nuc-1) at the viral long terminal repeats (LTR) such that the inhibition of histone deacetyltransferase and histone lysine methyltransferase activities, respectively, reactivates HIV from latency. Non-epigenetic mechanisms involve the nuclear restriction of critical cellular transcription factors such as nuclear factor-kappa beta (NF-κB) or nuclear factor of activated T-cells (NFAT) which activate transcription from the viral LTR, limiting the nuclear levels of the viral transcription transactivator protein Tat and its cellular co-factor positive transcription elongation factor b (P-TEFb), which together regulate HIV transcriptional elongation. In this article, we review how T-cell receptor (TCR) activation efficiently induces NF-κB, NFAT, and activator protein 1 (AP-1) transcription factors through multiple signal pathways and how these factors efficiently regulate HIV LTR transcription through the non-epigenetic mechanism. We further discuss how elongation factor P-TEFb, induced through an extracellular signal-regulated kinase (ERK)-dependent mechanism, regulates HIV transcriptional elongation before new Tat is synthesized and the role of AP-1 in the modulation of HIV transcriptional elongation through functional synergy with NF-κB. Furthermore, we discuss how TCR signaling induces critical post-translational modifications of the cyclin-dependent kinase 9 (CDK9) subunit of P-TEFb which enhances interactions between P-TEFb and the viral Tat protein and the resultant enhancement of HIV transcriptional elongation.

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Koizume, Shiro, Tomoko Takahashi, Mitsuyo Yoshihara, Yoshiyasu Nakamura, Wolfram Ruf, Katsuya Takenaka, Etsuko Miyagi, and Yohei Miyagi. "Cholesterol Starvation and Hypoxia Activate the FVII Gene via the SREBP1-GILZ Pathway in Ovarian Cancer Cells to Produce Procoagulant Microvesicles." Thrombosis and Haemostasis 119, no. 07 (May 5, 2019): 1058–71. http://dx.doi.org/10.1055/s-0039-1687876.

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AbstractInteraction between the transcription factors, hypoxia-inducible factor (HIF1α and HIF2α) and Sp1, mediates hypoxia-driven expression of FVII gene encoding coagulation factor VII (fVII) in ovarian clear cell carcinoma (CCC) cells. This mechanism is synergistically enhanced in response to serum starvation, a condition possibly associated with tumor hypoxia. This transcriptional response potentially results in venous thromboembolism, a common complication in cancer patients by producing procoagulant extracellular vesicles (EVs). However, which deficient serum factors are responsible for this characteristic transcriptional mechanism is unknown. Here, we report that cholesterol deficiency mediates synergistic FVII expression under serum starvation and hypoxia (SSH) via novel sterol regulatory element binding protein-1 (SREBP1)-driven mechanisms. Unlike conventional mechanisms, SREBP1 indirectly enhances FVII transcription through the induction of a new target, glucocorticoid-induced leucine zipper (GILZ) protein. GILZ expression induced in response to hypoxia by a HIF1α-dependent mechanism activates SREBP1 under SSH, suggesting reciprocal regulation between SREBP1 and GILZ. Furthermore, GILZ binds to the FVII locus. Xenograft tumor samples analyzed by chromatin immunoprecipitation confirmed that HIF1α-aryl hydrocarbon nuclear translocator and GILZ bind to the TSC22D3 (GILZ) and FVII gene loci, respectively, thereby potentially modulating chromatin function to augment FVII transcription. Thus, deficiency of both O2 and cholesterol, followed by interplay between HIFs, Sp1, and SREBP1-GILZ pathways synergistically induce fVII synthesis, resulting in the shedding of procoagulant EVs.

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Teng, Christina T. "Factors regulating lactoferrin gene expressionThis paper is one of a selection of papers published in this Special Issue, entitled 7th International Conference on Lactoferrin: Structure, Function, and Applications, and has undergone the Journal's usual peer review process." Biochemistry and Cell Biology 84, no. 3 (June 2006): 263–67. http://dx.doi.org/10.1139/o06-034.

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Regulation of gene expression by nuclear receptors and transcription factors involves the concerted action of multiple proteins. The process of transcriptional activation involves chromatin modification, nuclear receptor or transcription factor binding to the response element of the promoter, and coregulator recruitment. Despite advances in knowledge pertaining to the molecular mechanisms of gene regulation overall, there is very limited information available on the molecular mechanism of lactoferrin gene regulation. This review will outline novel information relating to general gene regulation and will discuss the current understanding of the regulation of lactoferrin gene expression by nuclear receptors and transcription factors.

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Zhang, Yuli, and Linlin Hou. "Alternate Roles of Sox Transcription Factors beyond Transcription Initiation." International Journal of Molecular Sciences 22, no. 11 (May 31, 2021): 5949. http://dx.doi.org/10.3390/ijms22115949.

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Sox proteins are known as crucial transcription factors for many developmental processes and for a wide range of common diseases. They were believed to specifically bind and bend DNA with other transcription factors and elicit transcriptional activation or repression activities in the early stage of transcription. However, their functions are not limited to transcription initiation. It has been showed that Sox proteins are involved in the regulation of alternative splicing regulatory networks and translational control. In this review, we discuss the current knowledge on how Sox transcription factors such as Sox2, Sry, Sox6, and Sox9 allow the coordination of co-transcriptional splicing and also the mechanism of SOX4-mediated translational control in the context of RNA polymerase III.

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Iyer, V., and K. Struhl. "Mechanism of differential utilization of the his3 TR and TC TATA elements." Molecular and Cellular Biology 15, no. 12 (December 1995): 7059–66. http://dx.doi.org/10.1128/mcb.15.12.7059.

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The yeast his3 promoter region contains two TATA elements, TC and TR, that are differentially utilized in constitutive his3 transcription and Gcn4-activated his3 transcription. TR contains the canonical TATAAA sequence, whereas TC is an extended region that lacks a conventional TATA sequence and does not support transcription in vitro. Surprisingly, differential his3 TATA-element utilization does not depend on specific properties of activator proteins but, rather, is determined by the overall level of his3 transcription. At low levels of transcription, the upstream TC is preferentially utilized, even though it is inherently a much weaker TATA element than TR. The TATA elements are utilized equally at intermediate levels, whereas TR is strongly preferred at high levels of transcription. This characteristic behavior can be recreated by replacing TC with moderately functional derivatives of a conventional TATA element, suggesting that TC is a collection of weak TATA elements. Analysis of promoters containing two biochemically defined TATA elements indicates that differential utilization occurs when the upstream TATA element is weaker than the downstream element. In other situations, the upstream TATA element is preferentially utilized in a manner that is independent of the overall level of transcription. Thus, in promoters containing multiple TATA elements, relative utilization not only depends on the quality and arrangement of the TATA elements but can vary with the overall level of transcriptional stimulation. We suggest that differential TATA utilization results from the combination of an intrinsic preference for the upstream element and functional saturation of weak TATA elements at low levels of transcriptional stimulation.

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Yue, Lei, Jie Li, Bing Zhang, Lei Qi, Zhihua Li, Fangqing Zhao, Lingyan Li, Xiaowei Zheng, and Xiuzhu Dong. "The conserved ribonuclease aCPSF1 triggers genome-wide transcription termination of Archaea via a 3′-end cleavage mode." Nucleic Acids Research 48, no. 17 (August 28, 2020): 9589–605. http://dx.doi.org/10.1093/nar/gkaa702.

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Abstract Transcription termination defines accurate transcript 3′-ends and ensures programmed transcriptomes, making it critical to life. However, transcription termination mechanisms remain largely unknown in Archaea. Here, we reported the physiological significance of the newly identified general transcription termination factor of Archaea, the ribonuclease aCPSF1, and elucidated its 3′-end cleavage triggered termination mechanism. The depletion of Mmp-aCPSF1 in Methanococcus maripaludis caused a genome-wide transcription termination defect and disordered transcriptome. Transcript-3′end-sequencing revealed that transcriptions primarily terminate downstream of a uridine-rich motif where Mmp-aCPSF1 performed an endoribonucleolytic cleavage, and the endoribonuclease activity was determined to be essential to the in vivo transcription termination. Co-immunoprecipitation and chromatin-immunoprecipitation detected interactions of Mmp-aCPSF1 with RNA polymerase and chromosome. Phylogenetic analysis revealed that the aCPSF1 orthologs are ubiquitously distributed among the archaeal phyla, and two aCPSF1 orthologs from Lokiarchaeota and Thaumarchaeota could replace Mmp-aCPSF1 to terminate transcription of M. maripaludis. Therefore, the aCPSF1 dependent termination mechanism could be widely employed in Archaea, including Lokiarchaeota belonging to Asgard Archaea, the postulated archaeal ancestor of Eukaryotes. Strikingly, aCPSF1-dependent archaeal transcription termination reported here exposes a similar 3′-cleavage mode as the eukaryotic RNA polymerase II termination, thus would shed lights on understanding the evolutionary linking between archaeal and eukaryotic termination machineries.

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Lv, Xiaoyang, Wei Sun, Shuangxia Zou, Ling Chen, Joram M. Mwacharo, and Jinyu Wang. "Characteristics of the BMP7 Promoter in Hu Sheep." Animals 9, no. 11 (October 28, 2019): 874. http://dx.doi.org/10.3390/ani9110874.

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The BMP7 gene is involved in the growth and development of hair follicles but its regulation mechanism is unclear. We studied the regulation mechanism of the BMP7 promoter by cloning the proximal promoter of BMP7 for bioinformatics analysis. A series of missing vectors was then constructed for dual-fluorescein activity detection based on the bioinformatics analysis results. We tested transcription-factor binding-site mutations and transcription factor over-expression to analyze the transcriptional regulation principle of the BMP7 promoter region. The upstream transcriptional regulatory region of the BMP7 gene proximal promoter was predicted by bioinformatics. There were −1216 bp to −1166 bp and −632 bp to −582 bp transcription initiation sites in the upstream transcriptional regulatory region of the BMP7 gene proximal promoter. The CpG islands’ distribution showed that there were many CpG islands at −549 bp to 1 bp. A dual-luciferase assay revealed high activity between −758 bp and −545 bp in the core region and a possible binding site for transcription factors SP1 and EGR1. The transcriptional activity of BMP7 was significantly decreased in the transcriptional regulatory region of the BMP7 after EGR1 and SP1 mutation. Transcription was significantly enhanced by over expression of the EGR1 transcription factor, which strongly suggests that EGR1 and SP1 play important roles in BMP7 regulation.

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Hirsch, Heather A., Gauri W. Jawdekar, Kang-Ae Lee, Liping Gu, and R. William Henry. "Distinct Mechanisms for Repression of RNA Polymerase III Transcription by the Retinoblastoma Tumor Suppressor Protein." Molecular and Cellular Biology 24, no. 13 (July 1, 2004): 5989–99. http://dx.doi.org/10.1128/mcb.24.13.5989-5999.2004.

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ABSTRACT The retinoblastoma (RB) protein represses global RNA polymerase III transcription of genes that encode nontranslated RNAs, potentially to control cell growth. However, RNA polymerase III-transcribed genes exhibit diverse promoter structures and factor requirements for transcription, and a universal mechanism explaining global repression is uncertain. We show that RB represses different classes of RNA polymerase III-transcribed genes via distinct mechanisms. Repression of human U6 snRNA (class 3) gene transcription occurs through stable promoter occupancy by RB, whereas repression of adenovirus VAI (class 2) gene transcription occurs in the absence of detectable RB-promoter association. Endogenous RB binds to a human U6 snRNA gene in both normal and cancer cells that maintain functional RB but not in HeLa cells whose RB function is disrupted by the papillomavirus E7 protein. Both U6 promoter association and transcriptional repression require the A/B pocket domain and C region of RB. These regions of RB contribute to U6 promoter targeting through numerous interactions with components of the U6 general transcription machinery, including SNAPC and TFIIIB. Importantly, RB also concurrently occupies a U6 promoter with RNA polymerase III during repression. These observations suggest a novel mechanism for RB function wherein RB can repress U6 transcription at critical steps subsequent to RNA polymerase III recruitment.

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Liu, Bo, Zhanjiang Yuan, Kazuyuki Aihara, and Luonan Chen. "Reinitiation enhances reliable transcriptional responses in eukaryotes." Journal of The Royal Society Interface 11, no. 97 (August 6, 2014): 20140326. http://dx.doi.org/10.1098/rsif.2014.0326.

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Gene transcription is a noisy process carried out by the transcription machinery recruited to the promoter. Noise reduction is a fundamental requirement for reliable transcriptional responses which in turn are crucial for signal transduction. Compared with the relatively simple transcription initiation in prokaryotes, eukaryotic transcription is more complex partially owing to its additional reinitiation mechanism. By theoretical analysis, we showed that reinitiation reduces noise in eukaryotic transcription independent of the transcription level. Besides, a higher reinitiation rate enables a stable scaffold complex an advantage in noise reduction. Finally, we showed that the coupling between scaffold formation and transcription can further reduce transcription noise independent of the transcription level. Furthermore, compared with the reinitiation mechanism, the noise reduction effect of the coupling can be of more significance in the case that the transcription level is low and the intrinsic noise dominates. Our results uncover a mechanistic route which eukaryotes may use to facilitate a more reliable response in the noisy transcription process.

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OGBOURNE, Steven, and Toni M. ANTALIS. "Transcriptional control and the role of silencers in transcriptional regulation in eukaryotes." Biochemical Journal 331, no. 1 (April 1, 1998): 1–14. http://dx.doi.org/10.1042/bj3310001.

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Mechanisms controlling transcription and its regulation are fundamental to our understanding of molecular biology and, ultimately, cellular biology. Our knowledge of transcription initiation and integral factors such as RNA polymerase is considerable, and more recently our understanding of the involvement of enhancers and complexes such as holoenzyme and mediator has increased dramatically. However, an understanding of transcriptional repression is also essential for a complete understanding of promoter structure and the regulation of gene expression. Transcriptional repression in eukaryotes is achieved through ‘silencers ’, of which there are two types, namely ‘silencer elements ’ and ‘negative regulatory elements ’ (NREs). Silencer elements are classical, position-independent elements that direct an active repression mechanism, and NREs are position-dependent elements that direct a passive repression mechanism. In addition, ‘repressors ’ are DNA-binding trasncription factors that interact directly with silencers. A review of the recent literature reveals that it is the silencer itself and its context within a given promoter, rather than the interacting repressor, that determines the mechanism of repression. Silencers form an intrinsic part of many eukaryotic promoters and, consequently, knowledge of their interactive role with enchancers and other transcriptional elements is essential for our understanding of gene regulation in eukaryotes.

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Tsukamoto, Kenji. "Unique mechanism of coronavirus mRNA transcription." Uirusu 46, no. 2 (1996): 99–107. http://dx.doi.org/10.2222/jsv.46.99.

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Cai, W. "Transcription-modulating drugs: mechanism and selectivity." Current Opinion in Biotechnology 7, no. 6 (December 1996): 608–15. http://dx.doi.org/10.1016/s0958-1669(96)80071-1.

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Selby, C., and A. Sancar. "Molecular mechanism of transcription-repair coupling." Science 260, no. 5104 (April 2, 1993): 53–58. http://dx.doi.org/10.1126/science.8465200.

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Gusarov, Ivan, and Evgeny Nudler. "The Mechanism of Intrinsic Transcription Termination." Molecular Cell 3, no. 4 (April 1999): 495–504. http://dx.doi.org/10.1016/s1097-2765(00)80477-3.

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Louet, J. F., C. Le May, J. P. Pégorier, J. F. Decaux, and J. Girard. "Regulation of liver carnitine palmitoyltransferase I gene expression by hormones and fatty acids." Biochemical Society Transactions 29, no. 2 (May 1, 2001): 310–16. http://dx.doi.org/10.1042/bst0290310.

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This brief review focuses on the transcriptional regulation of liver carnitine palmitoyltransferase I (L-CPT I) by pancreatic and thyroid hormones and by long-chain fatty acids (LCFA). Both glucagon and 3,3′,5-tri-iodothyronine (T3) enhanced the transcription of the gene encoding L-CPT I, whereas insulin had the opposite effect. Interestingly, the transcriptional effect of T3 required, in addition to the thyroid-responsive element, the co-operation of a sequence located in the first intron of L-CPT I gene. Non-esterified fatty acids rather than acyl-CoA ester or intramitochondrial metabolite were responsible for the transcriptional effect on the gene encoding LCPT I. It was shown that LCFA and peroxisome proliferators stimulated L-CPT I gene transcription by distinct mechanisms. Peroxisome proliferator stimulated L-CPT I gene transcription through a peroxisome-proliferator-responsive element (PPRE) located at -2846 bp, whereas LCFA induced L-CPT I gene transcription through a peroxisome-proliferator-activated receptor α (PPARα)-independent mechanism owing to a sequence located in the first intron of the gene.

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Yadon, Adam N., Daniel Van de Mark, Ryan Basom, Jeffrey Delrow, Iestyn Whitehouse, and Toshio Tsukiyama. "Chromatin Remodeling around Nucleosome-Free Regions Leads to Repression of Noncoding RNA Transcription." Molecular and Cellular Biology 30, no. 21 (August 30, 2010): 5110–22. http://dx.doi.org/10.1128/mcb.00602-10.

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ABSTRACT Nucleosome-free regions (NFRs) at the 5′ and 3′ ends of genes are general sites of transcription initiation for mRNA and noncoding RNA (ncRNA). The presence of NFRs within transcriptional regulatory regions and the conserved location of transcription start sites at NFRs strongly suggest that the regulation of NFRs profoundly affects transcription initiation. To date, multiple factors are known to facilitate transcription initiation by positively regulating the formation and/or size of NFRs in vivo. However, mechanisms to repress transcription by negatively regulating the size of NFRs have not been identified. We identified four distinct classes of NFRs located at the 5′ and 3′ ends of genes, within open reading frames (ORFs), and far from ORFs. The ATP-dependent chromatin-remodeling enzyme Isw2 was found enriched at all classes of NFRs. Analysis of RNA levels also demonstrated Isw2 is required to repress ncRNA transcription from many of these NFRs. Thus, by the systematic annotation of NFRs across the yeast genome and analysis of ncRNA transcription, we established, for the first time, a mechanism by which NFR size is negatively regulated to repress ncRNA transcription from NFRs. Finally, we provide evidence suggesting that one biological consequence of repression of ncRNA, by Isw2 or by the exosome, is prevention of transcriptional interference of mRNA.

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Doyen, Cécile-Marie, Woojin An, Dimitar Angelov, Vladimir Bondarenko, Flore Mietton, Vassily M. Studitsky, Ali Hamiche, Robert G. Roeder, Philippe Bouvet, and Stefan Dimitrov. "Mechanism of Polymerase II Transcription Repression by the Histone Variant macroH2A." Molecular and Cellular Biology 26, no. 3 (February 1, 2006): 1156–64. http://dx.doi.org/10.1128/mcb.26.3.1156-1164.2006.

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ABSTRACT macroH2A (mH2A) is an unusual histone variant consisting of a histone H2A-like domain fused to a large nonhistone region. In this work, we show that histone mH2A represses p300- and Gal4-VP16-dependent polymerase II transcription, and we have dissected the mechanism by which this repression is realized. The repressive effect of mH2A is observed at the level of initiation but not at elongation of transcription, and mH2A interferes with p300-dependent histone acetylation. The nonhistone region of mH2A is responsible for both the repression of initiation of transcription and the inhibition of histone acetylation. In addition, the presence of this domain of mH2A within the nucleosome is able to block nucleosome remodeling and sliding of the histone octamer to neighboring DNA segments by the remodelers SWI/SNF and ACF. These data unambiguously identify mH2A as a strong transcriptional repressor and show that the repressive effect of mH2A is realized on at least two different transcription activation chromatin-dependent pathways: histone acetylation and nucleosome remodeling.

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Ainbinder, Elena, Merav Revach, Orit Wolstein, Sandra Moshonov, Noam Diamant, and Rivka Dikstein. "Mechanism of Rapid Transcriptional Induction of Tumor Necrosis Factor Alpha-Responsive Genes by NF-κB." Molecular and Cellular Biology 22, no. 18 (September 15, 2002): 6354–62. http://dx.doi.org/10.1128/mcb.22.18.6354-6362.2002.

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ABSTRACT NF-κB induces the expression of genes involved in immune response, apoptosis, inflammation, and the cell cycle. Certain NF-κB-responsive genes are activated rapidly after the cell is stimulated by cytokines and other extracellular signals. However, the mechanism by which these genes are activated is not entirely understood. Here we report that even though NF-κB interacts directly with TAFIIs, induction of NF-κB by tumor necrosis factor alpha (TNF-α) does not enhance TFIID recruitment and preinitiation complex formation on some NF-κB-responsive promoters. These promoters are bound by the transcription apparatus prior to TNF-α stimulus. Using the immediate-early TNF-α-responsive gene A20 as a prototype promoter, we found that the constitutive association of the general transcription apparatus is mediated by Sp1 and that this is crucial for rapid transcriptional induction by NF-κB. In vitro transcription assays confirmed that NF-κB plays a postinitiation role since it enhances the transcription reinitiation rate whereas Sp1 is required for the initiation step. Thus, the consecutive effects of Sp1 and NF-κB on the transcription process underlie the mechanism of their synergy and allow rapid transcriptional induction in response to cytokines.

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Asanoma, Kazuo, Ge Liu, Takako Yamane, Yoko Miyanari, Tomoka Takao, Hiroshi Yagi, Tatsuhiro Ohgami, et al. "Regulation of the Mechanism ofTWIST1Transcription by BHLHE40 and BHLHE41 in Cancer Cells." Molecular and Cellular Biology 35, no. 24 (September 21, 2015): 4096–109. http://dx.doi.org/10.1128/mcb.00678-15.

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BHLHE40 and BHLHE41 (BHLHE40/41) are basic helix-loop-helix type transcription factors that play key roles in multiple cell behaviors. BHLHE40/41 were recently shown to be involved in an epithelial-to-mesenchymal transition (EMT). However, the precise mechanism of EMT control by BHLHE40/41 remains unclear. In the present study, we demonstrated that BHLHE40/41 expression was controlled in a pathological stage-dependent manner in human endometrial cancer (HEC). Ourin vitroassays showed that BHLHE40/41 suppressed tumor cell invasion. BHLHE40/41 also suppressed the transcription of the EMT effectorsSNAI1,SNAI2, andTWIST1. We identified the critical promoter regions ofTWIST1for its basal transcriptional activity. We elucidated that the transcription factor SP1 was involved in the basal transcriptional activity ofTWIST1and that BHLHE40/41 competed with SP1 for DNA binding to regulate gene transcription. This study is the first to report the detailed functions of BHLHE40 and BHLHE41 in the suppression of EMT effectorsin vitro. Our results suggest that BHLHE40/41 suppress tumor cell invasion by inhibiting EMT in tumor cells. We propose that BHLHE40/41 are promising markers to predict the aggressiveness of each HEC case and that molecular targeting strategies involving BHLHE40/41 and SP1 may effectively regulate HEC progression.

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Li, Jun, Shuyan Dai, Xiaojuan Chen, Xujun Liang, Lingzhi Qu, Longying Jiang, Ming Guo, et al. "Mechanism of forkhead transcription factors binding to a novel palindromic DNA site." Nucleic Acids Research 49, no. 6 (February 12, 2021): 3573–83. http://dx.doi.org/10.1093/nar/gkab086.

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Abstract Forkhead transcription factors bind a canonical consensus DNA motif, RYAAAYA (R = A/G, Y = C/T), as a monomer. However, the molecular mechanisms by which forkhead transcription factors bind DNA as a dimer are not well understood. In this study, we show that FOXO1 recognizes a palindromic DNA element DIV2, and mediates transcriptional regulation. The crystal structure of FOXO1/DIV2 reveals that the FOXO1 DNA binding domain (DBD) binds the DIV2 site as a homodimer. The wing1 region of FOXO1 mediates the dimerization, which enhances FOXO1 DNA binding affinity and complex stability. Further biochemical assays show that FOXO3, FOXM1 and FOXI1 also bind the DIV2 site as homodimer, while FOXC2 can only bind this site as a monomer. Our structural, biochemical and bioinformatics analyses not only provide a novel mechanism by which FOXO1 binds DNA as a homodimer, but also shed light on the target selection of forkhead transcription factors.

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Rehnmark, S., A. C. Bianco, J. D. Kieffer, and J. E. Silva. "Transcriptional and posttranscriptional mechanisms in uncoupling protein mRNA response to cold." American Journal of Physiology-Endocrinology and Metabolism 262, no. 1 (January 1, 1992): E58—E67. http://dx.doi.org/10.1152/ajpendo.1992.262.1.e58.

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Three mechanisms account for the rapid elevation and maintenance of uncoupling protein (UCP) mRNA levels in cold-exposed rats, namely, an increase in the rate of transcription initiation, an increase in the fraction of nascent UCP transcripts undergoing elongation, and stabilization of the mature UCP mRNA. The second mechanism precedes and outlasts the increase in the rate of UCP gene transcription, which is brisk but short lived. After 48 h of cold exposure, mature UCP mRNA levels are maintained elevated solely on the basis of stabilization, since the levels of both transcription initiation and fifth intron-containing transcripts (precursors) have returned to basal. Results in hypothyroid rats given 3,5,3'-triiodothyronine (T3) and in dispersed brown adipocytes show that T3 is involved both in the increase in UCP mRNA precursor level and stabilization of mature UCP mRNA. These mechanisms are rapidly reversed when the rats are returned to thermoneutrality. These coordinated transcriptional and post-transcriptional mechanisms modulating UCP gene expression ensure a rapid increase in the concentration of UCP and prevent further accumulation of the protein as physiologically adequate levels are attained.

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Gill, Jatinder Kaur, Andrea Maffioletti, Varinia García-Molinero, Françoise Stutz, and Julien Soudet. "Fine Chromatin-Driven Mechanism of Transcription Interference by Antisense Noncoding Transcription." Cell Reports 31, no. 5 (May 2020): 107612. http://dx.doi.org/10.1016/j.celrep.2020.107612.

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Phelps, Eric D., Dawn L. Updike, Elizabeth C. Bullen, Paula Grammas, and Eric W. Howard. "Transcriptional and posttranscriptional regulation of angiopoietin-2 expression mediated by IGF and PDGF in vascular smooth muscle cells." American Journal of Physiology-Cell Physiology 290, no. 2 (February 2006): C352—C361. http://dx.doi.org/10.1152/ajpcell.00050.2005.

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Angiopoietins play a significant role in vascular development and angiogenesis. Both angiopoietin-1 (Ang1) and angiopoietin-2 (Ang2) bind the receptor tyrosine kinase Tie2. However, while Ang1 signaling results in the stabilization of vessel structure, Ang2 has been linked to vascular instability. The ratio of these two Tie2 ligands is thus critical for vascular stability and remodeling. This study identifies a mechanism of growth factor-mediated reduction in Ang2 expression in vascular smooth muscle cells (VSMCs). In response to PDGF, VSMCs downregulated Ang2 mRNA levels by 75% within 4 h, with a subsequent decrease in Ang2 protein levels. Quantitation of endogenous transcription rates revealed that PDGF stimulation did not alter Ang2 transcription rates, but instead induced a posttranscriptional mechanism of rapid Ang2 mRNA destabilization. The Ang2 mRNA half-life was reduced by at least 50% after PDGF treatment. The PDGF-induced mRNA turnover mechanism was dependent on several MAPK pathways, including ERK and JNK. In contrast, IGF-I, which did not significantly activate ERK or JNK, stimulated increased Ang2 expression through transcriptional activation. These findings demonstrate that VSMCs adjust Ang2 expression through multiple mechanisms, including changes in transcription as well as posttranscriptional mRNA destabilization.

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Jackel, Jamie N., R. Cody Buchmann, Udit Singhal, and David M. Bisaro. "Analysis of Geminivirus AL2 and L2 Proteins Reveals a Novel AL2 Silencing Suppressor Activity." Journal of Virology 89, no. 6 (December 31, 2014): 3176–87. http://dx.doi.org/10.1128/jvi.02625-14.

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ABSTRACTBoth posttranscriptional and transcriptional gene silencing (PTGS and TGS, respectively) participate in defense against the DNA-containing geminiviruses. As a countermeasure, members of the genusBegomovirus(e.g.,Cabbage leaf curl virus) encode an AL2 protein that is both a transcriptional activator and a silencing suppressor. The related L2 protein ofBeet curly top virus(genusCurtovirus) lacks transcription activation activity. Previous studies showed that both AL2 and L2 suppress silencing by a mechanism that correlates with adenosine kinase (ADK) inhibition, while AL2 in addition activates transcription of cellular genes that negatively regulate silencing pathways. The goal of this study was to clarify the general means by which these viral proteins inhibit various aspects of silencing. We confirmed that AL2 inhibits systemic silencing spread by a mechanism that requires transcription activation activity. Surprisingly, we also found that reversal of PTGS and TGS by ADK inactivation depended on whether experiments were conducted in vegetative or reproductiveNicotiana benthamianaplants (i.e., before or after the vegetative-to-reproductive transition). While AL2 was able to reverse silencing in both vegetative and reproductive plants, L2 and ADK inhibition were effective only in vegetative plants. This suggests that silencing maintenance mechanisms can change during development or in response to stress. Remarkably, we also observed that AL2 lacking its transcription activation domain could reverse TGS in reproductive plants, revealing a third, previously unsuspected AL2 suppression mechanism that depends on neither ADK inactivation nor transcription activation.IMPORTANCERNA silencing in plants is a multivalent antiviral defense, and viruses respond by elaborating multiple and sometimes multifunctional proteins that inhibit various aspects of silencing. The studies described here add an additional layer of complexity to this interplay. By examining geminivirus AL2 and L2 suppressor activities, we show that L2 is unable to suppress silencing inNicotiana benthamianaplants that have undergone the vegetative-to-reproductive transition. As L2 was previously shown to be effective in matureArabidopsisplants, these results illustrate that silencing mechanisms can change during development or in response to stress in ways that may be species specific. The AL2 and L2 proteins are known to share a suppression mechanism that correlates with the ability of both proteins to inhibit ADK, while AL2 in addition can inhibit silencing by transcriptionally activating cellular genes. Here, we also provide evidence for a third AL2 suppression mechanism that depends on neither transcription activation nor ADK inactivation. In addition to revealing the remarkable versatility of AL2, this work highlights the utility of viral suppressors as probes for the analysis of silencing pathways.

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OKA, Hiroya, Takaaki KOJIMA, and Hideo NAKANO. "Analysis System of Transcriptional Mechanism Mediated by a Filamentous Fungal Transcription Factor." JOURNAL OF THE BREWING SOCIETY OF JAPAN 115, no. 6 (2020): 306–12. http://dx.doi.org/10.6013/jbrewsocjapan.115.306.

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Lin, Xia, Yao-Yun Liang, Baohua Sun, Min Liang, Yujiang Shi, F. Charles Brunicardi, Yang Shi, and Xin-Hua Feng. "Smad6 Recruits Transcription Corepressor CtBP To Repress Bone Morphogenetic Protein-Induced Transcription." Molecular and Cellular Biology 23, no. 24 (December 15, 2003): 9081–93. http://dx.doi.org/10.1128/mcb.23.24.9081-9093.2003.

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ABSTRACT Smad6 and Smad7 are inhibitory Smads induced by transforming growth factor β-Smad signal transduction pathways in a negative-feedback mechanism. Previously it has been thought that inhibitory Smads bind to the type I receptor and block the phosphorylation of receptor-activated Smads, thereby inhibiting the initiation of Smad signaling. Conversely, few studies have suggested the possible nuclear functions of inhibitory Smads. Here, we present compelling evidence demonstrating that Smad6 repressed bone morphogenetic protein-induced Id1 transcription through recruiting transcriptional corepressor C-terminal binding protein (CtBP). A consensus CtBP-binding motif, PLDLS, was identified in the linker region of Smad6. Our findings show that mutation in the motif abolished the Smad6 binding to CtBP and subsequently its repressor activity of transcription. We conclude that the nuclear functions and physical interaction of Smad6 and CtBP provide a novel mechanism for the transcriptional regulation by inhibitory Smads.

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Chen, Cai, and Ralf Bundschuh. "Quantitative models for accelerated protein dissociation from nucleosomal DNA." Nucleic Acids Research 42, no. 15 (August 11, 2014): 9753–60. http://dx.doi.org/10.1093/nar/gku719.

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Abstract Binding of transcription factors to their binding sites in promoter regions is the fundamental event in transcriptional gene regulation. When a transcription factor binding site is located within a nucleosome, the DNA has to partially unwrap from the nucleosome to allow transcription factor binding. This reduces the rate of transcription factor binding and is a known mechanism for regulation of gene expression via chromatin structure. Recently a second mechanism has been reported where transcription factor off-rates are dramatically increased when binding to target sites within the nucleosome. There are two possible explanations for such an increase in off-rate short of an active role of the nucleosome in pushing the transcription factor off the DNA: (i) for dimeric transcription factors the nucleosome can change the equilibrium between monomeric and dimeric binding or (ii) the nucleosome can change the equilibrium between specific and non-specific binding to the DNA. We explicitly model both scenarios and find that dimeric binding can explain a large increase in off-rate while the non-specific binding model cannot be reconciled with the large, experimentally observed increase. Our results suggest a general mechanism how nucleosomes increase transcription factor dissociation to promote exchange of transcription factors and regulate gene expression.

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Ochiai, Hiroshi, Tetsutaro Hayashi, Mana Umeda, Mika Yoshimura, Akihito Harada, Yukiko Shimizu, Kenta Nakano, et al. "Genome-wide kinetic properties of transcriptional bursting in mouse embryonic stem cells." Science Advances 6, no. 25 (June 2020): eaaz6699. http://dx.doi.org/10.1126/sciadv.aaz6699.

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Transcriptional bursting is the stochastic activation and inactivation of promoters, contributing to cell-to-cell heterogeneity in gene expression. However, the mechanism underlying the regulation of transcriptional bursting kinetics (burst size and frequency) in mammalian cells remains elusive. In this study, we performed single-cell RNA sequencing to analyze the intrinsic noise and mRNA levels for elucidating the transcriptional bursting kinetics in mouse embryonic stem cells. Informatics analyses and functional assays revealed that transcriptional bursting kinetics was regulated by a combination of promoter- and gene body–binding proteins, including the polycomb repressive complex 2 and transcription elongation factors. Furthermore, large-scale CRISPR-Cas9–based screening identified that the Akt/MAPK signaling pathway regulated bursting kinetics by modulating transcription elongation efficiency. These results uncovered the key molecular mechanisms underlying transcriptional bursting and cell-to-cell gene expression noise in mammalian cells.

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Vakulskas, Christopher A., Keith M. Brady, and Timothy L. Yahr. "Mechanism of Transcriptional Activation by Pseudomonas aeruginosa ExsA." Journal of Bacteriology 191, no. 21 (August 28, 2009): 6654–64. http://dx.doi.org/10.1128/jb.00902-09.

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ABSTRACT ExsA is a transcriptional activator of the Pseudomonas aeruginosa type III secretion system (T3SS). The T3SS consists of >40 genes organized within 10 transcriptional units, each of which is controlled by the transcriptional activator ExsA. ExsA-dependent promoters contain two adjacent ExsA binding sites that when occupied protect the −30 to −70 region from DNase I cleavage. The promoters also possess regions bearing strong resemblance to the consensus −10 and −35 regions of σ70-dependent promoters. The spacing distance between the putative −10 and −35 regions of ExsA-dependent promoters, however, is increased by 4 to 5 bp compared to that in typical σ70-dependent promoters. In the present study, we demonstrate that ExsA-dependent transcriptional activation requires a 21- or 22-bp spacer length between the −10 and −35 regions. Despite the atypical spacing in this region, in vitro transcription assays using σ70-saturated RNA polymerase holoenzyme (RNAP-σ70) confirm that ExsA-dependent promoters are indeed σ70 dependent. Potassium permanganate footprinting experiments indicate that ExsA facilitates an early step in transcriptional initiation. Although RNAP-σ70 binds to the promoters with low affinity in the absence of ExsA, the activator stimulates transcription by enhancing recruitment of RNAP-σ70 to the P exsC and P exsD promoters. Abortive initiation assays confirm that ExsA enhances the equilibrium binding constant for RNAP while having only a modest effect on the isomerization rate constant.

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Cholewa-Waclaw, Justyna, Ruth Shah, Shaun Webb, Kashyap Chhatbar, Bernard Ramsahoye, Oliver Pusch, Miao Yu, Philip Greulich, Bartlomiej Waclaw, and Adrian P. Bird. "Quantitative modelling predicts the impact of DNA methylation on RNA polymerase II traffic." Proceedings of the National Academy of Sciences 116, no. 30 (July 9, 2019): 14995–5000. http://dx.doi.org/10.1073/pnas.1903549116.

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Patterns of gene expression are primarily determined by proteins that locally enhance or repress transcription. While many transcription factors target a restricted number of genes, others appear to modulate transcription levels globally. An example is MeCP2, an abundant methylated-DNA binding protein that is mutated in the neurological disorder Rett syndrome. Despite much research, the molecular mechanism by which MeCP2 regulates gene expression is not fully resolved. Here, we integrate quantitative, multidimensional experimental analysis and mathematical modeling to indicate that MeCP2 is a global transcriptional regulator whose binding to DNA creates “slow sites” in gene bodies. We hypothesize that waves of slowed-down RNA polymerase II formed behind these sites travel backward and indirectly affect initiation, reminiscent of defect-induced shockwaves in nonequilibrium physics transport models. This mechanism differs from conventional gene-regulation mechanisms, which often involve direct modulation of transcription initiation. Our findings point to a genome-wide function of DNA methylation that may account for the reversibility of Rett syndrome in mice. Moreover, our combined theoretical and experimental approach provides a general method for understanding how global gene-expression patterns are choreographed.

Journal articles on the topic 'Transcription mechanism'

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