Journal articles: 'Transcriptional autoregulation'

1

De Siervi, Adriana, Paola De Luca, Jung S. Byun, Li Jun Di, Temesgen Fufa, Cynthia M. Haggerty, Elba Vazquez, Cristian Moiola, Dan L. Longo, and Kevin Gardner. "Transcriptional Autoregulation by BRCA1." Cancer Research 70, no. 2 (January 12, 2010): 532–42. http://dx.doi.org/10.1158/0008-5472.can-09-1477.

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Crews, Stephen T., and Joseph C. Pearson. "Transcriptional autoregulation in development." Current Biology 19, no. 6 (March 2009): R241—R246. http://dx.doi.org/10.1016/j.cub.2009.01.015.

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Hobert, Oliver. "Maintaining a memory by transcriptional autoregulation." Current Biology 21, no. 4 (February 2011): R146—R147. http://dx.doi.org/10.1016/j.cub.2011.01.005.

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Hearing, P., and T. Shenk. "Sequence-independent autoregulation of the adenovirus type 5 E1A transcription unit." Molecular and Cellular Biology 5, no. 11 (November 1985): 3214–21. http://dx.doi.org/10.1128/mcb.5.11.3214-3221.1985.

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The adenovirus E1A gene is known to be autoregulated at the level of transcription. Autoregulation was found to be mediated by products of the E1A 13S mRNA, which induced a fivefold increase in E1A transcription rate. Deletion analysis suggested that the autoregulation did not require any specific sequence in the E1A transcriptional control region. This conclusion was reinforced by the demonstration that a cellular alpha-globin gene substituted for the E1A gene on the adenovirus chromosome was also positively regulated by E1A gene products.

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Hearing, P., and T. Shenk. "Sequence-independent autoregulation of the adenovirus type 5 E1A transcription unit." Molecular and Cellular Biology 5, no. 11 (November 1985): 3214–21. http://dx.doi.org/10.1128/mcb.5.11.3214.

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The adenovirus E1A gene is known to be autoregulated at the level of transcription. Autoregulation was found to be mediated by products of the E1A 13S mRNA, which induced a fivefold increase in E1A transcription rate. Deletion analysis suggested that the autoregulation did not require any specific sequence in the E1A transcriptional control region. This conclusion was reinforced by the demonstration that a cellular alpha-globin gene substituted for the E1A gene on the adenovirus chromosome was also positively regulated by E1A gene products.

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Sassone-Corsi, Paolo, John C. Sisson, and Inder M. Verma. "Transcriptional autoregulation of the proto-oncogene fos." Nature 334, no. 6180 (July 1988): 314–19. http://dx.doi.org/10.1038/334314a0.

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7

MAGENHEIM, Judith, Rachel HERTZ, Ina BERMAN, Janna NOUSBECK, and Jacob BAR-TANA. "Negative autoregulation of HNF-4α gene expression by HNF-4α1." Biochemical Journal 388, no. 1 (May 10, 2005): 325–32. http://dx.doi.org/10.1042/bj20041802.

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HNF-4α (hepatocyte nuclear factor-4α) is required for tissue-specific expression of many of the hepatic, pancreatic, enteric and renal traits. Heterozygous HNF-4α mutants are inflicted by MODY-1 (maturity onset diabetes of the young type-1). HNF-4α expression is reported here to be negatively autoregulated by HNF-4α1 and to be activated by dominant-negative HNF-4α1. Deletion and chromatin immunoprecipitation analysis indicated that negative autoregulation by HNF-4α1 was mediated by its association with the TATA-less HNF-4α core promoter enriched in Sp1, but lacking DR-1 response elements. Also, negative autoregulation by HNF-4α1 was independent of its transactivation function, being similarly exerted by transcriptional-defective MODY-1 missense mutants of HNF-4α1, or under conditions of suppressing or enhancing HNF-4α activity by small heterodimer partner or by inhibiting histone deacetylase respectively. Negative autoregulation by HNF-4α1 was abrogated by overexpressed Sp1. Transcriptional suppression by HNF-4α1 independently of its transactivation function may extend the scope of its transcriptional activity to interference with docking of the pre-transcriptional initiation complex to TATA-less promoters.

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Delahodde, A., T. Delaveau, and C. Jacq. "Positive autoregulation of the yeast transcription factor Pdr3p, which is involved in control of drug resistance." Molecular and Cellular Biology 15, no. 8 (August 1995): 4043–51. http://dx.doi.org/10.1128/mcb.15.8.4043.

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Simultaneous resistance to an array of drugs with different cytotoxic activities is a property of Saccharomyces cerevisiae, in which the protein Pdr3p has recently been shown to play a role as a transcriptional regulator. We provide evidence that the yeast PDR3 gene, which encodes a zinc finger transcription factor implicated in certain drug resistance phenomena, is under positive autoregulation by Pdr3p. DNase I footprinting analyses using bacterially expressed Pdr3p showed specific recognition by this protein of at least two upstream activating sequences in the PDR3 promoter. The use of lacZ reporter constructs, a mutational analysis of the upstream activating sequences, as well as band shift experiments enabled the identification of two 5'TC CGCGGA3' sequence motifs in the PDR3 gene as consensus elements for the binding of Pdr3p. Several similar sequence motifs can be found in the promoter of PDR5, a gene encoding an ATP-dependent drug pump whose Pdr3p-induced overexpression is responsible for drug resistance phenomena. Recently one of these sequence elements was shown to be the target of Pdr3p to elevate the level of PDR5 transcription. Finally, we provide evidence in the absence of PDR1 for a PDR3-controlled transcriptional induction of the drug pump by cycloheximide and propose a model for the mechanism governing the transcriptional autoregulation of Pdr3p.

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Bell, Stephen D., and Stephen P. Jackson. "Mechanism of Autoregulation by an Archaeal Transcriptional Repressor." Journal of Biological Chemistry 275, no. 41 (July 18, 2000): 31624–29. http://dx.doi.org/10.1074/jbc.m005422200.

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10

Soncini, F. C., E. G. Véscovi, and E. A. Groisman. "Transcriptional autoregulation of the Salmonella typhimurium phoPQ operon." Journal of bacteriology 177, no. 15 (1995): 4364–71. http://dx.doi.org/10.1128/jb.177.15.4364-4371.1995.

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Conacci-Sorrell, Maralice, Inbal Simcha, Tamar Ben-Yedidia, Janna Blechman, Pierre Savagner, and Avri Ben-Ze'ev. "Autoregulation of E-cadherin expression by cadherin–cadherin interactions." Journal of Cell Biology 163, no. 4 (November 17, 2003): 847–57. http://dx.doi.org/10.1083/jcb.200308162.

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Transcriptional repression of E-cadherin, characteristic of epithelial to mesenchymal transition, is often found also during tumor cell invasion. At metastases, migratory fibroblasts sometimes revert to an epithelial phenotype, by a process involving regulation of the E-cadherin–β-catenin complex. We investigated the molecular basis of this regulation, using human colon cancer cells with aberrantly activated β-catenin signaling. Sparse cultures mimicked invasive tumor cells, displaying low levels of E-cadherin due to transcriptional repression of E-cadherin by Slug. Slug was induced by β-catenin signaling and, independently, by ERK. Dense cultures resembled a differentiated epithelium with high levels of E-cadherin and β-catenin in adherens junctions. In such cells, β-catenin signaling, ErbB-1/2 levels, and ERK activation were reduced and Slug was undetectable. Disruption of E-cadherin–mediated contacts resulted in nuclear localization and signaling by β-catenin, induction of Slug and inhibition of E-cadherin transcription, without changes in ErbB-1/2 and ERK activation. This autoregulation of E-cadherin by cell–cell adhesion involving Slug, β-catenin and ERK could be important in tumorigenesis.

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12

Irvine, K. D., J. Botas, S. Jha, R. S. Mann, and D. S. Hogness. "Negative autoregulation by Ultrabithorax controls the level and pattern of its expression." Development 117, no. 1 (January 1, 1993): 387–99. http://dx.doi.org/10.1242/dev.117.1.387.

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The Drosophila homeotic gene Ultrabithorax (Ubx) encodes transcriptional regulatory proteins (UBX) that specify thoracic and abdominal segmental identities. Ubx autoregulation was examined by manipulating UBX levels, both genetically and with an inducible transgene, and monitoring the effect of these manipulations on the expression of Ubx and Ubx-lacZ reporter genes. Positive autoregulation by Ubx is restricted to the visceral mesoderm, while in other tissues Ubx negatively autoregulates. In some cases, negative autoregulation stabilizes UBX levels, while in others it modulates the spatial and temporal patterns of UBX expression. This modulation of UBX expression may enable Ubx to specify distinct identities in different segments. The upstream control region of Ubx contains multiple autoregulatory elements for both positive and negative autoregulation.

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Bagchi, Gargi, Santosh Chauhan, Deepak Sharma, and Jaya Sivaswami Tyagi. "Transcription and autoregulation of the Rv3134c-devR-devS operon of Mycobacterium tuberculosis." Microbiology 151, no. 12 (December 1, 2005): 4045–53. http://dx.doi.org/10.1099/mic.0.28333-0.

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DevR is a transcriptional regulator that mediates the genetic response of Mycobacterium tuberculosis to oxygen limitation and nitric oxide exposure. devR is co-transcribed along with devS, which encodes its cognate sensor kinase, and an upstream gene, Rv3134c. The transcriptional activity of this operon was characterized by primer extension, transcriptional fusion and electrophoretic mobility shift assays (EMSAs) under aerobic conditions. Transcription start points (Tsps) were detected upstream of both Rv3134c and devR, and the major transcript was derived from upstream of Rv3134c. Sequences with similarity to sigma factor consensus elements and to DevR-binding motifs were detected in the vicinity of the Tsps by in silico analysis. EMSAs with promoter regions and DevR protein showed that DevR binds to its own promoters in a sequence-specific manner with differing affinities. Consistent with the primer extension and EMSA data, Rv3134c promoters, and not devR promoters, were determined to be the principal promoters of this operon using reporter assays performed in Mycobacterium smegmatis and Escherichia coli. Furthermore, DevR modulated the activity of both devR and Rv3134c promoters. From these findings it is inferred that the Rv3134c-devR-devS operon is transcribed from multiple promoters and is autoregulated.

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14

Murray, Philip J., Eleonore Ocana, Hedda A. Meijer, and Jacqueline Kim Dale. "Auto-Regulation of Transcription and Translation: Oscillations, Excitability and Intermittency." Biomolecules 11, no. 11 (October 22, 2021): 1566. http://dx.doi.org/10.3390/biom11111566.

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Several members of the Hes/Her family, conserved targets of the Notch signalling pathway, encode transcriptional repressors that dimerise, bind DNA and self-repress. Such autoinhibition of transcription can yield homeostasis and, in the presence of delays that account for processes such as transcription, splicing and transport, oscillations. Whilst previous models of autoinhibition of transcription have tended to treat processes such as translation as being unregulated (and hence linear), here we develop and explore a mathematical model that considers autoinhibition of transcription together with nonlinear regulation of translation. It is demonstrated that such a model can yield, in the absence of delays, nonlinear dynamical behaviours such as excitability, homeostasis, oscillations and intermittency. These results indicate that regulation of translation as well as transcription allows for a much richer range of behaviours than is possible with autoregulation of transcription alone. A number of experiments are suggested that would that allow for the signature of autoregulation of translation as well as transcription to be experimentally detected in a Notch signalling system.

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15

Wang, Dan, Marty W. Mayo, and Albert S. Baldwin Jr. "Basic fibroblast growth factor transcriptional autoregulation requires EGR-1." Oncogene 14, no. 19 (May 1997): 2291–99. http://dx.doi.org/10.1038/sj.onc.1201069.

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Suzaki, Takuya, and Hanna Nishida. "Autoregulation of Legume Nodulation by Sophisticated Transcriptional Regulatory Networks." Molecular Plant 12, no. 9 (September 2019): 1179–81. http://dx.doi.org/10.1016/j.molp.2019.07.008.

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17

Drissi, Hicham, Quyen Luc, Rauf Shakoori, Susana Chuva De Sousa Lopes, Je-Yong Choi, Anne Terry, Ming Hu, et al. "Transcriptional autoregulation of the bone related CBFA1/RUNX2 gene." Journal of Cellular Physiology 184, no. 3 (2000): 341–50. http://dx.doi.org/10.1002/1097-4652(200009)184:3<341::aid-jcp8>3.0.co;2-z.

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18

Gonzalo-Asensio, Jesús, Carlos Y. Soto, Ainhoa Arbués, Javier Sancho, María del Carmen Menéndez, María J. García, Brigitte Gicquel, and Carlos Martín. "The Mycobacterium tuberculosis phoPR Operon Is Positively Autoregulated in the Virulent Strain H37Rv." Journal of Bacteriology 190, no. 21 (August 29, 2008): 7068–78. http://dx.doi.org/10.1128/jb.00712-08.

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ABSTRACT The attenuated Mycobacterium tuberculosis H37Ra strain is an isogenic counterpart of the virulent paradigm strain H37Rv. Recently, a link between a point mutation in the PhoP transcriptional regulator and avirulence of H37Ra was established. Remarkably, a previous study demonstrated negative autoregulation of the phoP gene in H37Ra. These findings led us to study the transcriptional autoregulation of PhoP in the virulent H37Rv strain. In contrast to the negative autoregulation of PhoP previously published for H37Ra, our experiments using a phoP promoter-lacZ fusion showed that PhoP is positively autoregulated in both H37Rv and H37Ra compared with an H37Rv phoP deletion mutant constructed in this study. Using quantitative reverse transcription-PCR (RT-PCR) analysis, we showed that the phoP gene is transcribed at similar levels in H37Rv and H37Ra. Gel mobility shift and DNase I footprinting assays allowed us to identify the precise binding region of PhoP from H37Rv to the phoP promoter. We also carried out RT-PCR studies to demonstrate that phoP is transcribed together with the adjacent gene phoR, which codes for the cognate histidine kinase of the phoPR two-component system. In addition, quantitative RT-PCR studies showed that phoR is independently transcribed from a promoter possibly regulated by PhoP. Finally, we discuss the possible role in virulence of a single point mutation found in the phoP gene from the attenuated H37Ra strain but not in virulent members of the M. tuberculosis complex.

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Haydel, Shelley E., William H. Benjamin, Nancy E. Dunlap, and Josephine E. Clark-Curtiss. "Expression, Autoregulation, and DNA Binding Properties of the Mycobacterium tuberculosis TrcR Response Regulator." Journal of Bacteriology 184, no. 8 (April 15, 2002): 2192–203. http://dx.doi.org/10.1128/jb.184.8.2192-2203.2002.

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ABSTRACT The TrcRS two-component system of Mycobacterium tuberculosis is comprised of the TrcS histidine kinase and the TrcR response regulator, which is homologous to the OmpR class of DNA binding response regulators. Reverse transcription-PCRs with total RNA showed that the trcR and trcS two-component system genes are transcribed in broth-grown M. tuberculosis. Analysis of the trcR and trcS genes using various SCOTS (selective capture of transcribed sequences) probes also confirmed that these genes are expressed in broth-grown cultures and after 18 h of M. tuberculosis growth in cultured human primary macrophages. To determine if the TrcR response regulator is autoregulated, a trcR-lacZ fusion plasmid and a TrcR expression plasmid were cotransformed into Escherichia coli. Upon induction of the TrcR protein, there was a >500-fold increase in β-galactosidase activity from the trcR-lacZ fusion, indicating that TrcR is involved in transcriptional autoactivation. Gel mobility shift assays with the trcR promoter and TrcR established that the response regulator was autoregulating via direct binding. By use of a delimiting series of overlapping trcR PCR fragments in gel mobility shift assays with TrcR, an AT-rich region of the trcR promoter was shown to be essential for TrcR binding. Additionally, this AT-rich sequence was protected by TrcR in DNase I protection assays. To further analyze the role of the AT-rich region in TrcR autoregulation, the trcR promoter was mutated and analyzed in lacZ transcriptional fusions in the presence of TrcR. Alteration of the AT-rich sequence in the trcR promoter resulted in the loss of trcR transcriptional activation in the presence of TrcR. This report indicates that the M. tuberculosis TrcR response regulator activates its own expression by interacting with the AT-rich sequence of the trcR promoter.

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Nishikawa, Keizo, Makoto Kobayashi, Atsuko Masumi, Susan E. Lyons, Brant M. Weinstein, P. Paul Liu, and Masayuki Yamamoto. "Self-Association of Gata1 Enhances Transcriptional Activity In Vivo in Zebra Fish Embryos." Molecular and Cellular Biology 23, no. 22 (November 15, 2003): 8295–305. http://dx.doi.org/10.1128/mcb.23.22.8295-8305.2003.

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ABSTRACT Gata1 is a prototype transcription factor that regulates hematopoiesis, yet the molecular mechanisms by which Gata1 transactivates its target genes in vivo remain unclear. We previously showed, in transgenic zebra fish, that Gata1 autoregulates its own expression. In this study, we characterized the molecular mechanisms for this autoregulation by using mutations in the Gata1 protein which impair autoregulation. Of the tested mutations, replacement of six lysine residues with alanine (Gata1KA6), which inhibited self-association activity of Gata1, reduced the Gata1-dependent induction of reporter gene expression driven by the zebra fish gata1 hematopoietic regulatory domain (gata1 HRD). Furthermore, overexpression of wild-type Gata1 but not Gata1KA6 rescued the expression of Gata1 downstream genes in vlad tepes, a germ line gata1 mutant fish. Interestingly, both GATA sites in the double GATA motif in gata1 HRD were critical for the promoter activity and for binding of the self-associated Gata1 complex, whereas only the 3′-GATA site was required for Gata1 monomer binding. These results thus provide the first in vivo evidence that the ability of Gata1 to self-associate critically contributes to the autoregulation of the gata1 gene.

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Niesner, Uwe, Inka Albrecht, Marko Janke, Cornelia Doebis, Christoph Loddenkemper, Maria H. Lexberg, Katharina Eulenburg, et al. "Autoregulation of Th1-mediated inflammation by twist1." Journal of Experimental Medicine 205, no. 8 (July 28, 2008): 1889–901. http://dx.doi.org/10.1084/jem.20072468.

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The basic helix-loop-helix transcriptional repressor twist1, as an antagonist of nuclear factor κB (NF-κB)–dependent cytokine expression, is involved in the regulation of inflammation-induced immunopathology. We show that twist1 is expressed by activated T helper (Th) 1 effector memory (EM) cells. Induction of twist1 in Th cells depended on NF-κB, nuclear factor of activated T cells (NFAT), and interleukin (IL)-12 signaling via signal transducer and activator of transcription (STAT) 4. Expression of twist1 was transient after T cell receptor engagement, and increased upon repeated stimulation of Th1 cells. Imprinting for enhanced twist1 expression was characteristic of repeatedly restimulated EM Th cells, and thus of the pathogenic memory Th cells characteristic of chronic inflammation. Th lymphocytes from the inflamed joint or gut tissue of patients with rheumatic diseases, Crohn's disease or ulcerative colitis expressed high levels of twist1. Expression of twist1 in Th1 lymphocytes limited the expression of the cytokines interferon-γ, IL-2, and tumor necrosis factor-α, and ameliorated Th1-mediated immunopathology in delayed-type hypersensitivity and antigen-induced arthritis.

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22

Luo, Katherine Leisan, Ryan S. Underwood, and Iva Greenwald. "Positive autoregulation of lag-1 in response to LIN-12 activation in cell fate decisions during C. elegans reproductive system development." Development 147, no. 18 (August 24, 2020): dev193482. http://dx.doi.org/10.1242/dev.193482.

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ABSTRACTDuring animal development, ligand binding releases the intracellular domain of LIN-12/Notch by proteolytic cleavage to translocate to the nucleus, where it associates with the DNA-binding protein LAG-1/CSL to activate target gene transcription. We investigated the spatiotemporal regulation of LAG-1/CSL expression in Caenorhabditis elegans and observed that an increase in endogenous LAG-1 levels correlates with LIN-12/Notch activation in different cell contexts during reproductive system development. We show that this increase is via transcriptional upregulation by creating a synthetic endogenous operon, and identified an enhancer region that contains multiple LAG-1 binding sites (LBSs) embedded in a more extensively conserved high occupancy target (HOT) region. We show that these LBSs are necessary for upregulation in response to LIN-12/Notch activity, indicating that lag-1 engages in direct positive autoregulation. Deletion of the HOT region from endogenous lag-1 reduced LAG-1 levels and abrogated positive autoregulation, but did not cause hallmark cell fate transformations associated with loss of lin-12/Notch or lag-1 activity. Instead, later somatic reproductive system defects suggest that proper transcriptional regulation of lag-1 confers robustness to somatic reproductive system development.

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Esvald, Eli-Eelika, Jürgen Tuvikene, Alex Sirp, Sudarshan Patil, Clive R. Bramham, and Tõnis Timmusk. "CREB Family Transcription Factors Are Major Mediators of BDNF Transcriptional Autoregulation in Cortical Neurons." Journal of Neuroscience 40, no. 7 (January 8, 2020): 1405–26. http://dx.doi.org/10.1523/jneurosci.0367-19.2019.

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24

Masui, Toshihiko, Galvin H. Swift, Michael A. Hale, David M. Meredith, Jane E. Johnson, and Raymond J. MacDonald. "Transcriptional Autoregulation Controls Pancreatic Ptf1a Expression during Development and Adulthood." Molecular and Cellular Biology 28, no. 17 (July 7, 2008): 5458–68. http://dx.doi.org/10.1128/mcb.00549-08.

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ABSTRACT The basic helix-loop-helix (bHLH) transcription factor PTF1a is critical to the development of the embryonic pancreas. It is required early for the formation of the undifferentiated tubular epithelium of the nascent pancreatic rudiment and then becomes restricted to the differentiating acinar cells, where it directs the transcriptional activation of the secretory digestive enzyme genes. Here we report that the complex temporal and spatial expression of Ptf1a is controlled by at least three separable gene-flanking regions. A 14.8-kb control domain immediately downstream of the last Ptf1a exon is highly conserved among mammals and directs expression in the dorsal part of the spinal cord but has very little activity in the embryonic or neonatal pancreas. A 13.4-kb proximal promoter domain initiates limited expression in cells that begin the acinar differentiation program. The activity of the proximal promoter domain is complemented by an adjacent 2.3-kb autoregulatory enhancer that is able to activate a heterologous minimal promoter with high-level penetrance in the pancreases of transgenic mice. During embryonic development, the enhancer initiates expression in the early precursor epithelium and then superinduces expression in acinar cells at the onset of their development. The enhancer contains two evolutionarily conserved binding sites for the active form of PTF1a, a trimeric complex composed of PTF1a, one of the common bHLH E proteins, and either RBPJ or RBPJL. The two sites are essential for acinar cell-specific transcription in transfected cell lines and mice. In mature acinar cells, the enhancer and PTF1a establish an autoregulatory loop that reinforces and maintains Ptf1a expression. Indeed, the trimeric PTF1 complex forms dual autoregulatory loops with the Ptf1a and Rbpjl genes that may maintain the stable phenotype of pancreatic acinar cells.

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Croda-García, Gerardo, Victoria Grosso-Becerra, Abigail Gonzalez-Valdez, Luis Servín-González, and Gloria Soberón-Chávez. "Transcriptional regulation of Pseudomonas aeruginosa rhlR: role of the CRP orthologue Vfr (virulence factor regulator) and quorum-sensing regulators LasR and RhlR." Microbiology 157, no. 9 (September 1, 2011): 2545–55. http://dx.doi.org/10.1099/mic.0.050161-0.

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The production of many virulence factors by Pseudomonas aeruginosa is regulated by the quorum-sensing (QS) response. In this regulatory network LasR and RhlR, bound to their corresponding autoinducers, play a central role. The QS response has a hierarchical structure: LasR/3O-C12-HSL activates the transcription of rhlR, and RhlR/C4-HSL activates the transcription of several genes, including the rhlAB operon, which encodes the enzymes responsible for rhamnolipid synthesis. The rhlAB operon is located immediately upstream of the rhlR gene. rhlR has four transcription start sites, two of which are located in the rhlB coding region. Vfr directly activates transcription of lasR, and has been reported to be also involved in rhlR expression. The aim of this work was to characterize the details of the mechanism of rhlR transcriptional regulation. We show that Vfr directly regulates rhlR transcription through its binding to several Vfr-binding sites (VBSs) present in the rhlR promoter region, one of which has a negative effect on transcription. Two of the VBSs overlap with las boxes where LasR/3O-C12-HSL binds to activate rhlR transcription. We also show that rhlR transcription is subject to positive-feedback autoregulation through RhlR/C4-HSL activation of the rhlA promoter. This positive autoregulation plays a major role in rhlR expression.

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Wang, Kevin L. C., and Jonathan R. Warner. "Positive and Negative Autoregulation ofREB1 Transcription in Saccharomyces cerevisiae." Molecular and Cellular Biology 18, no. 7 (July 1, 1998): 4368–76. http://dx.doi.org/10.1128/mcb.18.7.4368.

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ABSTRACT Reb1p is a DNA binding protein of Saccharomyces cerevisiae that has been implicated in the activation of transcription by polymerase (Pol) II, in the termination of transcription by Pol I, and in the organization of nucleosomes. Studies of the transcriptional control of the REB1 gene have led us to identify three Reb1p binding sites in the 5′ region of the its gene, termed A, B, and C, at positions −110, −80, and +30 with respect to transcription initiation. In vitro, Reb1p binds to the three sites with the relative affinity of A ≥ C > B. Kinetic parameters suggest that when both A and C sites are present on the same DNA molecule, the C site may recruit Reb1p for the A site. In vivo the A and B sites each contribute to the transcription activity ofREB1 in roughly additive fashion. Mutation of both A and B sites abolishes transcription. On the other hand, the C site is a negative element, reducing transcription by 40%. In cells overexpressing Reb1p, the C site reduces transcription by more than 80%. This effect can be transposed to another transcription unit, demonstrating that the effect of Reb1p binding at the C site does not depend on interaction with upstream Reb1p molecules. Relocation of the C site to a position 105 bp downstream of the transcription initiation site abolishes its effect, suggesting that it does not act as a conventional attenuator of transcription. We conclude that binding of Reb1p at the C site hinders formation of the initiation complex. This arrangement of Reb1p binding sites provides a positive and negative mechanism to autoregulate the expression of REB1. Such an arrangement could serve to dampen the inevitable fluctuation in Rep1p levels caused by the intermittent presence of its mRNA within an individual cell.

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Brodhagen, Marion, Marcella D. Henkels, and Joyce E. Loper. "Positive Autoregulation and Signaling Properties of Pyoluteorin, an Antibiotic Produced by the Biological Control Organism Pseudomonas fluorescens Pf-5." Applied and Environmental Microbiology 70, no. 3 (March 2004): 1758–66. http://dx.doi.org/10.1128/aem.70.3.1758-1766.2004.

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ABSTRACT Pseudomonas fluorescens Pf-5, a rhizosphere bacterium, produces a suite of secondary metabolites that are toxic to seed- and root-rotting plant pathogens. Among these are the polyketide compounds pyoluteorin and 2,4-diacetylphloroglucinol. We provide evidence that pyoluteorin production is influenced by positive autoregulation. Addition of pyoluteorin to liquid cultures of Pf-5 enhanced pyoluteorin production. In addition, pyoluteorin and 2,4-diacetylphloroglucinol mutually inhibit one another's production in Pf-5. For pyoluteorin, both positive autoregulation and negative influences on production by 2,4-diacetylphloroglucinol were demonstrated at the transcriptional level by measuring activity from transcriptional fusions of an ice nucleation reporter gene (inaZ) to three separate pyoluteorin biosynthetic genes. The occurrence of pyoluteorin autoregulation in the rhizosphere was assessed on cucumber seedlings in pasteurized soil with cross-feeding experiments. In the rhizosphere, expression of a pyoluteorin biosynthesis gene by a pyoluteorin-deficient mutant of Pf-5 was enhanced by pyoluteorin produced by coinoculated cells of Pf-5. These data establish that the polyketide pyoluteorin is an autoregulatory compound and functions as a signal molecule influencing the spectrum of secondary metabolites produced by the bacterial cell.

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Ajdić, Dragana, and Joseph J. Ferretti. "Transcriptional Regulation of theStreptococcus mutans gal Operon by the GalR Repressor." Journal of Bacteriology 180, no. 21 (November 1, 1998): 5727–32. http://dx.doi.org/10.1128/jb.180.21.5727-5732.1998.

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ABSTRACT The galactose operon of Streptococcus mutans is transcriptionally regulated by a repressor protein (GalR) encoded by the galR gene, which is divergently oriented from the structural genes of the gal operon. To study the regulatory function of GalR, we partially purified the protein and examined its DNA binding activity by gel mobility shift and DNase I footprinting experiments. The protein specifically bound to thegalR-galK intergenic region at an operator sequence, the position of which would suggest that GalR plays a role in the regulation of the gal operon as well as autoregulation. To further examine this hypothesis, transcriptional start sites of the gal operon and thegalR gene were determined. Primer extension analysis showed that both promoters overlap the operator, indicating that GalR most likely represses transcription initiation of both promoters. Finally, the results from in vitro binding experiments with potential effector molecules suggest that galactose is a true intracellular inducer of the galactose operon.

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Franco, Elisa, Giulia Giordano, Per-Ola Forsberg, and Richard M. Murray. "Negative Autoregulation Matches Production and Demand in Synthetic Transcriptional Networks." ACS Synthetic Biology 3, no. 8 (April 3, 2014): 589–99. http://dx.doi.org/10.1021/sb400157z.

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Ban, Hiroyuki, Daisuke Yokota, Shiori Otosaka, Morimichi Kikuchi, Hirofumi Kinoshita, Yuuri Fujino, Taijiro Yabe, et al. "Transcriptional autoregulation of zebrafish tbx6 is required for somite segmentation." Development 146, no. 18 (August 23, 2019): dev177063. http://dx.doi.org/10.1242/dev.177063.

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Casalino, Laura, Dario De Cesare, and Pasquale Verde. "Accumulation of Fra-1 in ras-Transformed Cells Depends on Both Transcriptional Autoregulation and MEK-Dependent Posttranslational Stabilization." Molecular and Cellular Biology 23, no. 12 (June 15, 2003): 4401–15. http://dx.doi.org/10.1128/mcb.23.12.4401-4415.2003.

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ABSTRACT The AP-1 transcription factor plays an essential role in cell proliferation and tumorigenesis. It was previously shown that the fra-1 gene product is upregulated by various oncogenes and is involved in the in vitro and in vivo transformation of thyroid cells. Here we show that the ras oncogene-dependent accumulation of Fra-1 is mediated by a positive feedback mechanism which requires both transcriptional autoregulation and posttranslational stabilization of the protein. The oncogene-dependent transcriptional activation involves the cooperation between both Raf-dependent and Raf-independent pathways and is mediated by an AP-1 site within the fra-1 first intron, which becomes stably occupied by a transcriptionally active Fra-1-containing complex in ras-transformed cells. The posttranslational stabilization results in a drastic increase in the Fra-1 half-life in ras-transformed cells and is totally dependent on the activity of the MEK/ERK phosphorylation pathway. The analysis of the Fra-1 transactivation potential shows that the protein is able to stimulate a heterologous promoter in a ras-dependent manner, but the transactivating activity requires the recruitment of a heterodimeric partner. These data show that the alteration of multiple regulatory mechanisms is required for the constitutive activation of Fra-1 as a nuclear target of ras transformation.

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Hoffmann, Bernd, Oliver Valerius, Meike Andermann, and Gerhard H. Braus. "Transcriptional Autoregulation and Inhibition of mRNA Translation of Amino Acid Regulator GenecpcAof Filamentous FungusAspergillus nidulans." Molecular Biology of the Cell 12, no. 9 (September 2001): 2846–57. http://dx.doi.org/10.1091/mbc.12.9.2846.

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The CPCA protein of the filamentous fungus Aspergillus nidulans is a member of the c-Jun-like transcriptional activator family. It acts as central transcription factor of the cross-pathway regulatory network of amino acid biosynthesis and is functionally exchangeable for the general control transcriptional activator Gcn4p of Saccharomyces cerevisiae. In contrast to GCN4, expression of cpcA is strongly regulated by two equally important mechanisms with additive effects that lead to a fivefold increased CPCA protein amount under amino acid starvation conditions. One component of cpcA regulation involves a transcriptional autoregulatory mechanism via a CPCA recognition element (CPRE) in the cpcA promoter that causes a sevenfold increased cpcA mRNA level when cells are starved for amino acids. Point mutations in the CPRE cause a constitutively low mRNA level of cpcA and a halved protein level when amino acids are limited. Moreover, two upstream open reading frames (uORFs) in the 5′ region of thecpcA mRNA are important for a translational regulatory mechanism. Destruction of both short uORFs results in a sixfold increased CPCA protein level under nonstarvation conditions and a 10-fold increase under starvation conditions. Mutations in both the CPRE and uORF regulatory elements lead to an intermediate effect, with a low cpcA mRNA level but a threefold increased CPCA protein level independent of amino acid availability. These data argue for a combined regulation of cpcA that includes a translational regulation like that of yeast GCN4 as well as a transcriptional regulation like that of the mammalianjun and fos genes.

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Timchenko, N., D. R. Wilson, L. R. Taylor, S. Abdelsayed, M. Wilde, M. Sawadogo, and G. J. Darlington. "Autoregulation of the human C/EBP alpha gene by stimulation of upstream stimulatory factor binding." Molecular and Cellular Biology 15, no. 3 (March 1995): 1192–202. http://dx.doi.org/10.1128/mcb.15.3.1192.

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The human C/EBP alpha gene promoter shares significant sequence homology with that of the mouse but has a different mechanism of autoregulation. Activation of the murine promoter by direct binding of C/EBP alpha to a site within 200 bp of the transcriptional start was shown to elevate activity by approximately threefold (R. J. Christy, K. H. Kaestner, D. E. Geiman, and M. D. Lane, Proc. Natl. Acad. Sci. USA 88:2593-2597, 1991; K. Legraverend, P. Antonson, P. Flodby, and K. G. Xanthapoulos, Nucleic Acids Res. 21:1735-1742, 1993). Unlike its murine counterpart, the human C/EBP alpha gene promoter does not contain a cis element that binds the C/EBP alpha protein. Neither C/EBP alpha nor C/EBP beta (NF-Il-6) binds the human C/EBP alpha promoter within 437 bp. However, cotransfection studies show that C/EBP alpha stimulates transcription of a reporter gene driven by 437 bp of the C/EBP alpha promoter. Our studies show that the human C/EBP alpha protein stimulates USF to bind to a USF consensus element within C/EBP alpha promoter and activates it by two- to threefold. We propose that the human gene employs the ubiquitously expressed DNA-binding protein factor USF to carry out autoregulation. Autoregulation of the human C/EBP alpha promoter was abolished by deletion of the USF binding site, CACGTG. Expression of human C/EBP beta following transfection did not stimulate USF binding. These studies suggest a mechanism whereby tissue-specific autoregulation can be achieved via a trans-acting factor that is expressed in all cell types. Thus, direct binding of the C/EBP alpha protein to the promoter of the C/EBP alpha gene is not required for autoregulation.

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Martínez, Marta, José M. Palacios, Juan Imperial, and Tomás Ruiz-Argüeso. "Symbiotic Autoregulation of nifA Expression in Rhizobium leguminosarum bv. viciae." Journal of Bacteriology 186, no. 19 (October 1, 2004): 6586–94. http://dx.doi.org/10.1128/jb.186.19.6586-6594.2004.

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ABSTRACT NifA is the general transcriptional activator of nitrogen fixation genes in diazotrophic bacteria. In Rhizobium leguminosarum bv. viciae UPM791, the nifA gene is part of a gene cluster (orf71 orf79 fixW orf5 fixABCX nifAB) separated by 896 bp from an upstream and divergent truncated duplication of nifH (ΔnifH). Symbiotic expression analysis of genomic nifA::lacZ fusions revealed that in strain UPM791 nifA is expressed mainly from a σ54-dependent promoter (P nifA1 ) located upstream of orf71. This promoter contains canonical NifA upstream activating sequences located 91 bp from the transcription initiation site. The transcript initiated in P nifA1 spans 5.1 kb and includes nifA and nifB genes. NifA from Klebsiella pneumoniae was able to activate transcription from P nifA1 in a heterologous Escherichia coli system. In R. leguminosarum, the P nifA1 promoter is essential for effective nitrogen fixation in symbiosis with peas. In its absence, partially efficient nitrogen-fixing nodules were produced, and the corresponding bacteroids exhibited only low levels of nifA gene expression. The basal level of nifA expression resulted from a promoter activity originating upstream of the fixX-nifA intergenic region and probably from an incomplete duplication of P nifA1 located immediately upstream of fixA.

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Newton, A., N. Ohta, G. Ramakrishnan, D. Mullin, and G. Raymond. "Genetic switching in the flagellar gene hierarchy of Caulobacter requires negative as well as positive regulation of transcription." Proceedings of the National Academy of Sciences 86, no. 17 (September 1989): 6651–55. http://dx.doi.org/10.1073/pnas.86.17.6651.

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Caulobacter crescentus flagellar (fla, flb, or flg) genes are periodically expressed in the cell cycle and they are organized in a regulatory hierarchy. We have analyzed the genetic interactions required for fla gene expression by determining the effect of mutations in 30 known fla genes on transcription from four operons in the hook gene cluster. These results show that the flaO (transcription unit III) and flbF (transcription unit IV) operons are located at or near the top of the hierarchy. They also reveal an extensive network of negative transcriptional controls that are superimposed on the positive regulatory cascade described previously. The strong negative autoregulation observed for the flaN (transcription unit I), flbG (transcription unit II), and flaO (transcription unit III) promoters provides one possible mechanism for turning off fla gene expression at the end of the respective synthetic periods. We suggest that these positive and negative transcriptional interactions are components of genetic switches that determine the sequence in which fla genes are turned on and off in the C. crescentus cell cycle.

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Morales, Sergio E., and Thomas A. Lewis. "Transcriptional Regulation of the pdt Gene Cluster of Pseudomonas stutzeri KC Involves an AraC/XylS Family Transcriptional Activator (PdtC) and the Cognate Siderophore Pyridine-2,6-Bis(Thiocarboxylic Acid)." Applied and Environmental Microbiology 72, no. 11 (August 25, 2006): 6994–7002. http://dx.doi.org/10.1128/aem.01518-06.

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ABSTRACT In order to gain an understanding of the molecular mechanisms dictating production of the siderophore and dechlorination agent pyridine-2,6-bis(thiocarboxylic acid) (PDTC), we have begun characterization of a gene found in the pdt gene cluster of Pseudomonas stutzeri KC predicted to have a regulatory role. That gene product is an AraC family transcriptional activator, PdtC. Quantitative reverse transcription-PCR and expression of transcriptional reporter fusions were used to assess a role for pdtC in the transcription of pdt genes. PdtC and an upstream, promoter-proximal DNA segment were required for wild-type levels of expression from the promoter of a predicted biosynthesis operon (P pdt F ). At least two other transcriptional units within the pdt cluster were also dependent upon pdtC for expression at wild-type levels. The use of a heterologous, Pseudomonas putida host demonstrated that pdtC and an exogenously added siderophore were necessary and sufficient for expression from the pdtF promoter, i.e., none of the PDTC utilization genes within the pdt cluster were required for transcriptional signaling. Tests using the promoter of the pdtC gene in transcriptional reporter fusions indicated siderophore-dependent negative autoregulation similar to that seen with other AraC-type regulators of siderophore biosynthesis and utilization genes. The data increase the repertoire of siderophore systems known to be regulated by this type of transcriptional activator and have implications for PDTC signaling.

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Ottaviano, Daniela, Chiara Micolonghi, Lorenza Tizzani, Marc Lemaire, Micheline Wésolowski-Louvel, Maria Egle De Stefano, Danilo Ranieri, and Michele M. Bianchi. "Autoregulation of the Kluyveromyces lactis pyruvate decarboxylase gene KlPDC1 involves the regulatory gene RAG3." Microbiology 160, no. 7 (July 1, 2014): 1369–78. http://dx.doi.org/10.1099/mic.0.078543-0.

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In the yeast Kluyveromyces lactis, the pyruvate decarboxylase gene KlPDC1 is strongly regulated at the transcription level by different environmental factors. Sugars and hypoxia act as inducers of transcription, while ethanol acts as a repressor. Their effects are mediated by gene products, some of which have been characterized. KlPDC1 transcription is also strongly repressed by its product – KlPdc1 – through a mechanism called autoregulation. We performed a genetic screen that allowed us to select and identify the regulatory gene RAG3 as a major factor in the transcriptional activity of the KlPDC1 promoter in the absence of the KlPdc1 protein, i.e. in the autoregulatory mechanism. We also showed that the two proteins Rag3 and KlPdc1 interact, co-localize in the cell and that KlPdc1 may control Rag3 nuclear localization.

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Kędzierska, Barbara, Katarzyna Potrykus, Agnieszka Szalewska-Pałasz, and Beata Wodzikowska. "Insights into Transcriptional Repression of the Homologous Toxin-Antitoxin Cassettes yefM-yoeB and axe-txe." International Journal of Molecular Sciences 21, no. 23 (November 28, 2020): 9062. http://dx.doi.org/10.3390/ijms21239062.

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Transcriptional repression is a mechanism which enables effective gene expression switch off. The activity of most of type II toxin-antitoxin (TA) cassettes is controlled in this way. These cassettes undergo negative autoregulation by the TA protein complex which binds to the promoter/operator sequence and blocks transcription initiation of the TA operon. Precise and tight control of this process is vital to avoid uncontrolled expression of the toxin component. Here, we employed a series of in vivo and in vitro experiments to establish the molecular basis for previously observed differences in transcriptional activity and repression levels of the pyy and pat promoters which control expression of two homologous TA systems, YefM-YoeB and Axe-Txe, respectively. Transcriptional fusions of promoters with a lux reporter, together with in vitro transcription, EMSA and footprinting assays revealed that: (1) the different sequence composition of the −35 promoter element is responsible for substantial divergence in strengths of the promoters; (2) variations in repression result from the TA repressor complex acting at different steps in the transcription initiation process; (3) transcription from an additional promoter upstream of pat also contributes to the observed inefficient repression of axe-txe module. This study provides evidence that even closely related TA cassettes with high sequence similarity in the promoter/operator region may employ diverse mechanisms for transcriptional regulation of their genes.

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Jean-Pierre, Fabrice, Jonathan Perreault, and Eric Déziel. "Complex autoregulation of the post-transcriptional regulator RsmA in Pseudomonas aeruginosa." Microbiology 161, no. 9 (September 1, 2015): 1889–96. http://dx.doi.org/10.1099/mic.0.000140.

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40

Oei, Shiao Li, Herbert Herzog, Monica Hirsch-Kauffmann, Rainer Schneider, Bernhard Auer, and Manfred Schweiger. "Transcriptional regulation and autoregulation of the human gene for ADP-ribosyltransferase." Molecular and Cellular Biochemistry 138, no. 1-2 (1994): 99–104. http://dx.doi.org/10.1007/bf00928449.

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Reuner, Karl Heinrich, Matthias Wiederhold, Petra Dunker, Ingo Just, Rainer Maria Bohle, Manfred Kroger, and Norbert Katz. "Autoregulation of Actin Synthesis in Hepatocytes by Transcriptional and Posttranscriptional Mechanisms." European Journal of Biochemistry 230, no. 1 (May 1995): 32–37. http://dx.doi.org/10.1111/j.1432-1033.1995.0032i.x.

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Bode, Nadine J., Kun-Wei Chan, Xiang-Peng Kong, and Melanie M. Pearson. "Distinct Residues Contribute to Motility Repression and Autoregulation in the Proteus mirabilis Fimbria-Associated Transcriptional Regulator AtfJ." Journal of Bacteriology 198, no. 15 (May 31, 2016): 2100–2112. http://dx.doi.org/10.1128/jb.00193-16.

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ABSTRACTProteus mirabiliscontributes to a significant number of catheter-associated urinary tract infections, where coordinated regulation of adherence and motility is critical for ascending disease progression. Previously, the mannose-resistantProteus-like (MR/P) fimbria-associated transcriptional regulator MrpJ has been shown to both repress motility and directly induce the transcription of its own operon; in addition, it affects the expression of a wide range of cellular processes. Interestingly, 14 additionalmrpJparalogs are included in theP. mirabilisgenome. Looking at a selection of MrpJ paralogs, we discovered that these proteins, which consistently repress motility, also have nonidentical functions that include cross-regulation of fimbrial operons. A subset of paralogs, including AtfJ (encoded by the ambient temperature fimbrial operon), Fim8J, and MrpJ, are capable of autoinduction. We identified an element of theatfpromoter extending from 487 to 655 nucleotides upstream of the transcriptional start site that is responsive to AtfJ, and we found that AtfJ directly binds this fragment. Mutational analysis of AtfJ revealed that its two identified functions, autoregulation and motility repression, are not invariably linked. Residues within the DNA-binding helix-turn-helix domain are required for motility repression but not necessarily autoregulation. Likewise, the C-terminal domain is dispensable for motility repression but is essential for autoregulation. Supported by a three-dimensional (3D) structural model, we hypothesize that the C-terminal domain confers unique regulatory capacities on the AtfJ family of regulators.IMPORTANCEBalancing adherence with motility is essential for uropathogens to successfully establish a foothold in their host.Proteus mirabilisuses a fimbria-associated transcriptional regulator to switch between these antagonistic processes by increasing fimbrial adherence while simultaneously downregulating flagella. The discovery of multiple related proteins, many of which also function as motility repressors, encoded in theP. mirabilisgenome has raised considerable interest as to their functionality and potential redundancy in this organism. This study provides an important advance in this field by elucidating the nonidentical effects of these paralogs on a molecular level. Our mechanistic studies of one member of this group, AtfJ, shed light on how these differing functions may be conferred despite the limited sequence variety exhibited by the paralogous proteins.

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Reeves, Matthew, Jane Murphy, Richard Greaves, Jennifer Fairley, Alex Brehm, and John Sinclair. "Autorepression of the Human Cytomegalovirus Major Immediate-Early Promoter/Enhancer at Late Times of Infection Is Mediated by the Recruitment of Chromatin Remodeling Enzymes by IE86." Journal of Virology 80, no. 20 (October 15, 2006): 9998–10009. http://dx.doi.org/10.1128/jvi.01297-06.

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ABSTRACT The human cytomegalovirus major immediate-early protein IE86 is pivotal for coordinated regulation of viral gene expression throughout infection. A relatively promiscuous transactivator of viral early and late gene transcription, IE86 also acts during infection to negatively regulate its own promoter via direct binding to a 14-bp palindromic IE86-binding site, the cis repression sequence (crs), located between the major immediate-early promoter (MIEP) TATA box and the start of transcription. Although such autoregulation does not involve changes in the binding of basal transcription factors to the MIEP in vitro, it does appear to involve selective inhibition of RNA polymerase II recruitment. However, how this occurs is unclear. We show that autorepression by IE86 at late times of infection correlates with changes in chromatin structure around the MIEP during the course of infection and that this is likely to result from physical and functional interactions between IE86 and chromatin remodeling enzymes normally associated with transcriptional repression of cellular promoters. Firstly, we show that IE86-mediated autorepression is inhibited by histone deacetylase inhibitors. We also show that IE86 interacts, in vitro and in vivo, with the histone deacetylase HDAC1 and histone methyltransferases G9a and Suvar(3-9)H1 and that coexpression of these chromatin remodeling enzymes with IE86 increases autorepression of the MIEP. Finally, we show that mutation of the crs in the context of the virus abrogates the transcriptionally repressive chromatin phenotype normally found around the MIEP at late times of infection, suggesting that negative autoregulation by IE86 results, at least in part, from IE86-mediated changes in chromatin structure of the viral MIEP.

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Liptay, S., R. M. Schmid, E. G. Nabel, and G. J. Nabel. "Transcriptional regulation of NF-kappa B2: evidence for kappa B-mediated positive and negative autoregulation." Molecular and Cellular Biology 14, no. 12 (December 1994): 7695–703. http://dx.doi.org/10.1128/mcb.14.12.7695-7703.1994.

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NF-kappa B is an inducible transcription factor complex which regulates the expression of a variety of genes which are involved in the immune, inflammatory, and acute-phase responses. The maintenance of NF-kappa B activity in stimulated cells requires ongoing protein synthesis, suggesting several modes of regulation. In this report, we have characterized the transcriptional regulation of one family member, NF-kappa B2. The genomic structure and sequence of NF-kappa B2 revealed the presence of two promoters and at least four kappa B regulatory elements, which mediate responsiveness to phorbol myristate acetate and tumor necrosis factor alpha. Similar to other NF-kappa B family members, NF-kappa B2 is positively autoregulated. In contrast to other family members, we find that kappa B elements in the NFKB2 promoter can also mediate transcriptional repression in the absence of NF-kappa B. We identified a nuclear complex which binds specifically to a subset of kappa B-related sites but not to the canonical kappa B element. Because of its putative inhibitory or repressive effect, this binding activity has been termed Rep-kappa B. This mechanism of repressing basal NF-kappa B2 transcription in an inactivated state enables the cell to tightly control NF-kappa B2 activity. These data demonstrate that a novel mode of kappa B-dependent regulation is mediated by specific kappa B sites in the NFKB2 promoter.

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Liptay, S., R. M. Schmid, E. G. Nabel, and G. J. Nabel. "Transcriptional regulation of NF-kappa B2: evidence for kappa B-mediated positive and negative autoregulation." Molecular and Cellular Biology 14, no. 12 (December 1994): 7695–703. http://dx.doi.org/10.1128/mcb.14.12.7695.

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NF-kappa B is an inducible transcription factor complex which regulates the expression of a variety of genes which are involved in the immune, inflammatory, and acute-phase responses. The maintenance of NF-kappa B activity in stimulated cells requires ongoing protein synthesis, suggesting several modes of regulation. In this report, we have characterized the transcriptional regulation of one family member, NF-kappa B2. The genomic structure and sequence of NF-kappa B2 revealed the presence of two promoters and at least four kappa B regulatory elements, which mediate responsiveness to phorbol myristate acetate and tumor necrosis factor alpha. Similar to other NF-kappa B family members, NF-kappa B2 is positively autoregulated. In contrast to other family members, we find that kappa B elements in the NFKB2 promoter can also mediate transcriptional repression in the absence of NF-kappa B. We identified a nuclear complex which binds specifically to a subset of kappa B-related sites but not to the canonical kappa B element. Because of its putative inhibitory or repressive effect, this binding activity has been termed Rep-kappa B. This mechanism of repressing basal NF-kappa B2 transcription in an inactivated state enables the cell to tightly control NF-kappa B2 activity. These data demonstrate that a novel mode of kappa B-dependent regulation is mediated by specific kappa B sites in the NFKB2 promoter.

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Zhou, P., and D. J. Thiele. "Rapid transcriptional autoregulation of a yeast metalloregulatory transcription factor is essential for high-level copper detoxification." Genes & Development 7, no. 9 (September 1, 1993): 1824–35. http://dx.doi.org/10.1101/gad.7.9.1824.

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Barendt, Skye, Cierra Birch, Lea Mbengi, and Peter Zuber. "Evidence that Oxidative Stress InducesspxA2Transcription in Bacillus anthracis Sterne through a Mechanism Requiring SpxA1 and Positive Autoregulation." Journal of Bacteriology 198, no. 21 (August 8, 2016): 2902–13. http://dx.doi.org/10.1128/jb.00512-16.

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ABSTRACTBacillus anthracispossesses two paralogs of the transcriptional regulator, Spx. SpxA1 and SpxA2 interact with RNA polymerase (RNAP) to activate the transcription of genes implicated in the prevention and alleviation of oxidative protein damage. ThespxA2gene is highly upregulated in infected macrophages, but how this is achieved is unknown. Previous studies have shown that thespxA2gene was under negative control by the Rrf2 family repressor protein, SaiR, whose activity is sensitive to oxidative stress. These studies also suggested thatspxA2was under positive autoregulation. In the present study, we show byin vivoandin vitroanalyses thatspxA2is under direct autoregulation but is also dependent on the SpxA1 paralogous protein. The deletion of eitherspxA1orspxA2reduced the diamide-inducible expression of anspxA2-lacZconstruct.In vitrotranscription reactions using purifiedB. anthracisRNAP showed that SpxA1 and SpxA2 protein stimulates transcription from a DNA fragment containing thespxA2promoter. Ectopically positionedspxA2-lacZfusion requires both SpxA1 and SpxA2 for expression, but the requirement for SpxA1 is partially overcome whensaiRis deleted. Electrophoretic mobility shift assays showed that SpxA1 and SpxA2 enhance the affinity of RNAP forspxA2promoter DNA and that this activity is sensitive to reductant. We hypothesize that the previously observed upregulation ofspxA2in the oxidative environment of the macrophage is at least partly due to SpxA1-mediated SaiR repressor inactivation and the positive autoregulation ofspxA2transcription.IMPORTANCERegulators of transcription initiation are known to govern the expression of genes required for virulence in pathogenic bacterial species. Members of the Spx family of transcription factors function in control of genes required for virulence and viability in low-GC Gram-positive bacteria. InBacillus anthracis, thespxA2gene is highly induced in infected macrophages, which suggests an important role in the control of virulence gene expression during the anthrax disease state. We provide evidence that elevated concentrations of oxidized, active SpxA2 result from an autoregulatory positive-feedback loop drivingspxA2transcription.

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Shroff, Robert A., Robin A. Lockington, and Joan M. Kelly. "Analysis of mutations in the creA gene involved in carbon catabolite repression in Aspergillus nidulans." Canadian Journal of Microbiology 42, no. 9 (September 1, 1996): 950–59. http://dx.doi.org/10.1139/m96-122.

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The molecular nature of a number of creA mutant alleles has been determined. Three alleles analysed are missense mutations in the DNA binding domain and predicted to reduce but not abolish binding. Of the other four alleles, two result from frameshifts: one has a nonsense mutation and the other has an inversion. All four alleles result in truncations of the protein after the zinc finger domain, such that the protein no longer contains at least the carboxy terminal 145 amino acids, so identifying a region required for repression. Transcriptional analysis of creA indicates that the transcript is autoregulated and analysis using 5′ rapid amplification of cDNA ends indicates that transcriptional start points exist in clusters over a region of 200 bp located up to 595 bp 5′ of the translational start point. The two major clusters have potential CREA-binding sites (SYGGRG) at appropriate positions to allow autoregulation. Autoregulation leads to the creA transcript being most abundant in carbon catabolite nonrepressing conditions, and this, together with the phenotypes of the mutant alleles, has led to the suggestion that CREA has effects under conditions generally not considered as carbon catabolite repressing, as well as in carbon catabolite repressing conditions.Key words: carbon catabolite repression, MIG1, CREA, zinc finger protein, transcriptional repressor.

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Liu, Guang-Hui, Jing Qu, and Xun Shen. "Thioredoxin-mediated Negative Autoregulation of Peroxisome Proliferator-activated Receptor α Transcriptional Activity." Molecular Biology of the Cell 17, no. 4 (April 2006): 1822–33. http://dx.doi.org/10.1091/mbc.e05-10-0979.

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PPARα, a member of the nuclear receptor superfamily, and thioredoxin, a critical redox-regulator in cells, were found to form a negative feedback loop, which autoregulates transcriptional activity of PPARα. Thioredoxin was identified as a target gene of PPARα. Activation of PPARα leads to increase of thioredoxin expression as well as its translocation from cytoplasm to nucleus, whereas ectopic overexpression of thioredoxin in the nucleus dramatically inhibited both constitutive and ligand-dependent PPARα activation. As PPARα-target genes, the expression of muscle carnitine palmitoyltransferase I, medium chain acyl CoA dehydrogenase, and apolipoprotein A-I were significantly down-regulated by nucleus-targeted thioredoxin at transcriptional or protein level. The suppression of PPARα transcriptional activity by Trx could be enhanced by overexpression of thioredoxin reductase or knockdown of thioredoxin-interacting protein, but abrogated by mutating the redox-active sites of thioredoxin. Mammalian one-hybrid assays showed that thioredoxin inhibited PPARα activity by modulating its AF-1 transactivation domain. It was also demonstrated by electrophoretic mobility-shift assay that thioredoxin inhibited the binding of PPARα to the PPAR-response element. Together, it is speculated that the reported negative-feedback loop may be essential for maintaining the homeostasis of PPARα activity.

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Hao, Tong, Dvora Biran, Gregory J. Velicer, and Lee Kroos. "Identification of the Ω4514 Regulatory Region, a Developmental Promoter of Myxococcus xanthus That Is Transcribed In Vitro by the Major Vegetative RNA Polymerase." Journal of Bacteriology 184, no. 12 (June 15, 2002): 3348–59. http://dx.doi.org/10.1128/jb.184.12.3348-3359.2002.

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ABSTRACT Ω4514 is the site of a Tn5 lac insertion in the Myxococcus xanthus genome that fuses lacZ expression to a developmentally regulated promoter. DNA upstream of the insertion site was cloned, and the promoter was localized. The promoter resembles vegetative promoters in sequence, and σA RNA polymerase, the major form of RNA polymerase in growing M. xanthus, initiated transcription from this promoter in vitro. Two complete open reading frames were identified downstream of the promoter and before the Ω4514 insertion. The first gene product (ORF1) has a putative helix-turn-helix DNA-binding motif and shows sequence similarity to transcriptional regulators. ORF2 is most similar to subunit A of glutaconate coenzyme A (CoA) transferase, which is involved in glutamate fermentation. Tn5 lac Ω4514 is inserted in the third codon of ORF3, which is similar to subunit B of glutaconate CoA-transferase. An orf1 disruption mutant exhibited a mild sporulation defect, whereas neither a disruption of orf2 nor insertion Ω4514 in orf3 caused a defect. Based on DNA sequence analysis, the three genes are likely to be cotranscribed with a fourth gene whose product is similar to alcohol dehydrogenases. ORF1 delays and reduces expression of the operon during development, but relief from this negative autoregulation does not fully explain the regulation of the operon, because expression from a small promoter-containing fragment is strongly induced during development of an orf1 mutant. Also, multiple upstream DNA elements are necessary for full developmental expression. These results suggest that transcriptional activation also regulates the operon. Ω4514 is the first example of a developmentally regulated M. xanthus operon that is transcribed by the major vegetative RNA polymerase, and its regulation appears to involve both negative autoregulation by ORF1 and positive regulation by one or more transcriptional activators.

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Journal articles on the topic 'Transcriptional autoregulation'

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