scholarly journals Transcription factor IIIA gene expression in Xenopus oocytes utilizes a transcription factor similar to the major late transcription factor.

1989 ◽  
Vol 9 (11) ◽  
pp. 5003-5011 ◽  
Author(s):  
R K Hall ◽  
W L Taylor
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Transcriptional Control ◽  
Somatic Cells ◽  
State Level ◽  
Control Element ◽  
Transcription Factor Iiia ◽  
Shift Analysis ◽  
Late Transcription ◽  
Upstream Element

Xenopus transcription factor IIIA (TFIIIA) gene expression is stringently regulated during development. The steady-state level of TFIIIA mRNA in a somatic cell is approximately 10(6) times less than in an immature oocyte. We have undertaken studies designed to identify differences in how the TFIIIA gene is transcribed in oocytes and somatic cells. In this regard, we have localized an upstream transcriptional control element in the TFIIIA promoter that stimulates transcription from the TFIIIA promoter approximately threefold in microinjected oocytes. The upstream element, in cis. does not stimulate transcription from the TFIIIA promoter in somatic cells. Thus, the element appears to be oocyte specific in the context of the TFIIIA promoter. However, both oocytes and somatic cells contain a protein (or a related protein) that binds the upstream element. We have termed this protein from oocytes the TFIIIA distal element factor. The sequence of the upstream element is similar to the sequence of the upstream element found in the adenovirus major late promoter that is a binding site for the major late transcription factor. By gel shift analysis, chemical footprinting, methylation intereference, and point mutation analysis, we demonstrate that the TFIIIA distal element factor and major late transcription factor have similar DNA-binding properties.

Transcription factor IIIA gene expression in Xenopus oocytes utilizes a transcription factor similar to the major late transcription factor

1989 ◽  
Vol 9 (11) ◽  
pp. 5003-5011
Author(s):  
R K Hall ◽  
W L Taylor
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Transcriptional Control ◽  
Somatic Cells ◽  
State Level ◽  
Control Element ◽  
Transcription Factor Iiia ◽  
Shift Analysis ◽  
Late Transcription ◽  
Upstream Element

Xenopus transcription factor IIIA (TFIIIA) gene expression is stringently regulated during development. The steady-state level of TFIIIA mRNA in a somatic cell is approximately 10(6) times less than in an immature oocyte. We have undertaken studies designed to identify differences in how the TFIIIA gene is transcribed in oocytes and somatic cells. In this regard, we have localized an upstream transcriptional control element in the TFIIIA promoter that stimulates transcription from the TFIIIA promoter approximately threefold in microinjected oocytes. The upstream element, in cis. does not stimulate transcription from the TFIIIA promoter in somatic cells. Thus, the element appears to be oocyte specific in the context of the TFIIIA promoter. However, both oocytes and somatic cells contain a protein (or a related protein) that binds the upstream element. We have termed this protein from oocytes the TFIIIA distal element factor. The sequence of the upstream element is similar to the sequence of the upstream element found in the adenovirus major late promoter that is a binding site for the major late transcription factor. By gel shift analysis, chemical footprinting, methylation intereference, and point mutation analysis, we demonstrate that the TFIIIA distal element factor and major late transcription factor have similar DNA-binding properties.

scholarly journals EGR1 transcriptional control of human cytomegalovirus latency

2019 ◽  
Author(s):  
Jason Buehler ◽  
Ethan Carpenter ◽  
Sebastian Zeltzer ◽  
Suzu Igarashi ◽  
Michael Rak ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Human Cytomegalovirus ◽  
Transcriptional Control ◽  
Viral Reactivation ◽  
Erk Signaling ◽  
Viral Gene ◽  
Egfr Signaling ◽  
Down Regulation ◽  
Cmv Reactivation

ABSTRACTSustained phosphotinositide3-kinase (PI3K) signaling is critical to the maintenance of herpesvirus latency. We have previously shown that the beta-herpesvirus, human cytomegalovirus (CMV), regulates epidermal growth factor receptor (EGFR), upstream of PI3K, to control states of latency and reactivation. Inhibition of EGFR signaling enhances CMV reactivation from latency and increases viral replication, but the mechanisms by which EGFR impacts replication and latency is not known. We demonstrate that HCMV downregulates MEK/ERK and AKT phosphorylation, but not STAT3 or PLCγ for productive replication. Similarly, inhibition of either MEK/ERK or PI3K/AKT, but not STAT or PLCγ, pathways increases viral reactivation from latently infected CD34+hematopoietic progenitor cells (HPCs), defining a role for these pathways in latency. We hypothesized that CMV modulation of EGFR signaling might impact viral transcription. Indeed, EGF-stimulation increased expression of theUL138latency gene, but not immediate early or early viral genes, suggesting that EGFR signaling promotes latent gene expression. The early growth response-1 (EGR1) transcription factor is induced downstream of EGFR signaling through both PI3K/AKT and MEK/ERK pathways. EGR1 expression is important for the maintenance of HPC stemness and its downregulation drives HPC differentiation and mobilization. We demonstrate that EGR1 binds upstream ofUL138and is sufficient to promoteUL138expression. Further, disruption of EGR1 binding upstream ofUL138prevented CMV from establishing a latent infection in CD34+HPCs. Our results indicate a model whereby UL138 modulation of EGFR signaling feeds back to promote UL138 expression and suppression of replication to establish or maintain viral quiescence.AUTHOR SUMMARYCMV regulates EGFR signaling to balance states of viral latency and replication. CMV blocks downstream PI3K/AKT and MEK/ERK signaling pathways through down-regulation of EGFR at the plasma membrane. PI3K/AKT and MEK/ERK signaling increases expression of the EGR1 transcription factor that is necessary for the maintenance of stem cell stemness. A decrease in EGR1 expression promotes HPC mobilization to the periphery and differentiation, a known stimulus for CMV reactivation. We identified functional EGR1 binding sites upstream of theUL138gene and EGR-1 binding stimulatesUL138expression. Additionally, down-regulation of EGR1 by CMV miR-US22 decreasesUL138expression emphasizing the importance of this transcription factor in expression of this latency gene. Lastly, we demonstrate that a CMV mutant virus lacking an upstream EGR1 binding site is unable to establish latency in CD34+HPCs. This study defines one mechanism by which EGFR signaling impacts viral gene expression to promote CMV latency.

scholarly journals Homeobox Genes and Melatonin Synthesis: Regulatory Roles of the Cone-Rod Homeobox Transcription Factor in the Rodent Pineal Gland

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Kristian Rohde ◽  
Morten Møller ◽  
Martin Fredensborg Rath
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Circadian Rhythm ◽  
Pineal Gland ◽  
Transcriptional Control ◽  
Homeobox Genes ◽  
Control Mechanisms ◽  
Camp Response Element ◽  
Homeobox Transcription Factor ◽  
Melatonin Production

Nocturnal synthesis of melatonin in the pineal gland is controlled by a circadian rhythm in arylalkylamine N-acetyltransferase (AANAT) enzyme activity. In the rodent,Aanatgene expression displays a marked circadian rhythm; release of norepinephrine in the gland at night causes a cAMP-based induction ofAanattranscription. However, additional transcriptional control mechanisms exist. Homeobox genes, which are generally known to encode transcription factors controlling developmental processes, are also expressed in the mature rodent pineal gland. Among these, the cone-rod homeobox (CRX) transcription factor is believed to control pineal-specificAanatexpression. Based on recent advances in our understanding ofCrxin the rodent pineal gland, we here suggest that homeobox genes play a role in adult pineal physiology both by ensuring pineal-specificAanatexpression and by facilitating cAMP response element-based circadian melatonin production.

scholarly journals Regulation of α-Fetoprotein Expression by Nkx2.8

2002 ◽  
Vol 22 (17) ◽  
pp. 6122-6130 ◽  
Author(s):  
Yasuo Kajiyama ◽  
Jianmin Tian ◽  
Joseph Locker
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Regulatory Region ◽  
Mrna Translation ◽  
Nuclear Extract ◽  
Orphan Nuclear Receptor ◽  
Developmentally Regulated ◽  
Shift Analysis ◽  
Gene Reactivation ◽  
Afp Promoter

ABSTRACT The α-fetoprotein (AFP) gene is an important model of developmental gene silencing and neoplastic gene reactivation. Nkx2.8 is a divergent homeodomain factor originally cloned through its binding to the promoter-coupling element (PCE), a regulatory region upstream of the AFP promoter that mediates stimulation by distant enhancers. Nkx2.8 is the only developmentally regulated factor that has been associated with AFP gene expression. Fetoprotein transcription factor, an orphan nuclear receptor, has also been shown to bind the PCE but is not developmentally regulated. The binding specificities of both families of transcription factor were determined, and overlapping sites for each were defined in the PCE. After modification of nuclear extract and gel shift analysis procedures, Nkx2.8 was identified in six AFP-positive cell lines. Transient-transfection analysis did not show transcriptional stimulation by Nkx2.8 or other active NK2 factors, which only interfered with gene expression. However, two sets of analysis demonstrated the relationship of Nkx2.8 to AFP expression: chromatin immunoprecipitation demonstrated that Nkx2.8 bound to the active AFP promoter, and antisense inhibition of Nkx2.8 mRNA translation selectively reduced expression of both the endogenous human AFP gene and transfected reporters containing the rat AFP promoter.

MCM1 binds to a transcriptional control element in Ty1

1993 ◽  
Vol 13 (1) ◽  
pp. 57-62
Author(s):  
B Errede
Keyword(s):  
Gene Expression ◽  
Transcriptional Control ◽  
Control Element ◽  
Regulatory Sequence ◽  
Gene Promoters ◽  
Adjacent Gene ◽  
Transposable Element Insertion ◽  
Transcriptional Regulatory ◽  
Transcriptional Regulatory Sequence ◽  
Insertion Mutations

Some Ty1 transposable-element insertion mutations of Saccharomyces cerevisiae activate adjacent-gene expression. These Ty1-activated genes are regulated similarly to certain mating genes. This report shows that the MCM1 protein, which binds to several mating genes, also binds to a transcriptional regulatory sequence in Ty1. The binding of MCM1 to Ty1 correlates with the ability of its binding site to function as a component of the Ty1 transcriptional activator. This correlation supports the idea that MCM1 is important for Ty1-activated gene expression. At mating-gene promoters, MCM1 binds with coactivators or repressors such as STE12, alpha 1, or alpha 2. In contrast, MCM1 binds without these associated DNA-binding proteins at its site in Ty1. This finding suggests that its role in Ty1-mediated transcription is different from that at mating genes.

scholarly journals Transcriptional Control of Synaptic Plasticity by Transcription Factor NF-κB

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Christian Engelmann ◽  
Ronny Haenold
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Synaptic Plasticity ◽  
Transcriptional Control ◽  
Memory Formation ◽  
Inhibitory Synapses ◽  
Cross Sectional ◽  
Learning Deficits ◽  
Altered Gene

Activation of nuclear factor kappa B (NF-κB) transcription factors is required for the induction of synaptic plasticity and memory formation. All components of this signaling pathway are localized at synapses, and transcriptionally active NF-κB dimers move to the nucleus to translate synaptic signals into altered gene expression. Neuron-specific inhibition results in altered connectivity of excitatory and inhibitory synapses and functionally in selective learning deficits. Recent research on transgenic mice with impaired or hyperactivated NF-κB gave important insights into plasticity-related target gene expression that is regulated by NF-κB. In this minireview, we update the available data on the role of this transcription factor for learning and memory formation and comment on cross-sectional activation of NF-κB in the aged and diseased brain that may directly or indirectly affectκB-dependent transcription of synaptic genes.

scholarly journals MCM1 binds to a transcriptional control element in Ty1.

1993 ◽  
Vol 13 (1) ◽  
pp. 57-62 ◽  
Author(s):  
B Errede
Keyword(s):  
Gene Expression ◽  
Transcriptional Control ◽  
Control Element ◽  
Regulatory Sequence ◽  
Gene Promoters ◽  
Adjacent Gene ◽  
Transposable Element Insertion ◽  
Transcriptional Regulatory ◽  
Transcriptional Regulatory Sequence ◽  
Insertion Mutations

Some Ty1 transposable-element insertion mutations of Saccharomyces cerevisiae activate adjacent-gene expression. These Ty1-activated genes are regulated similarly to certain mating genes. This report shows that the MCM1 protein, which binds to several mating genes, also binds to a transcriptional regulatory sequence in Ty1. The binding of MCM1 to Ty1 correlates with the ability of its binding site to function as a component of the Ty1 transcriptional activator. This correlation supports the idea that MCM1 is important for Ty1-activated gene expression. At mating-gene promoters, MCM1 binds with coactivators or repressors such as STE12, alpha 1, or alpha 2. In contrast, MCM1 binds without these associated DNA-binding proteins at its site in Ty1. This finding suggests that its role in Ty1-mediated transcription is different from that at mating genes.

Dynamic competition between a ligand and transcription factor NusA governs riboswitch-mediated transcription regulation

2021 ◽  
Vol 118 (47) ◽  
pp. e2109026118
Author(s):  
Adrien Chauvier ◽  
Pujan Ajmera ◽  
Rajeev Yadav ◽  
Nils G. Walter
Keyword(s):  
Transcription Factor ◽  
Transcription Regulation ◽  
Single Molecule ◽  
Transcriptional Control ◽  
Response Times ◽  
Fast Response ◽  
Control Element ◽  
Order Structure ◽  
Control Of Gene Expression ◽  
Bacterial Transcription

Cotranscriptional RNA folding is widely assumed to influence the timely control of gene expression, but our understanding remains limited. In bacteria, the fluoride (F−)-sensing riboswitch is a transcriptional control element essential to defend against toxic F− levels. Using this model riboswitch, we find that its ligand F− and essential bacterial transcription factor NusA compete to bind the cotranscriptionally folding RNA, opposing each other’s modulation of downstream pausing and termination by RNA polymerase. Single-molecule fluorescence assays probing active transcription elongation complexes discover that NusA unexpectedly binds highly reversibly, frequently interrogating the complex for emerging, cotranscriptionally folding RNA duplexes. NusA thus fine-tunes the transcription rate in dependence of the ligand-responsive higher-order structure of the riboswitch. At the high NusA concentrations found intracellularly, this dynamic modulation is expected to lead to adaptive bacterial transcription regulation with fast response times.

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