scholarly journals A Novel Function for Human Rad9 Protein as a Transcriptional Activator of Gene Expression

Cell Cycle ◽  
2004 ◽  
Vol 3 (8) ◽  
pp. 1006-1008 ◽  
Author(s):  
Howard B. Lieberman ◽  
Yuxin Yin
Keyword(s):  
Gene Expression ◽  
Transcriptional Activator ◽  
Human Rad9

scholarly journals RovC - a novel type of hexameric transcriptional activator promoting type VI secretion gene expression

2020 ◽  
Vol 16 (9) ◽  
pp. e1008552 ◽  
Author(s):  
Vanessa Knittel ◽  
Pooja Sadana ◽  
Stephanie Seekircher ◽  
Anne-Sophie Stolle ◽  
Britta Körner ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcriptional Activator ◽  
Type Vi Secretion

scholarly journals Quantitative Control of Noise in Mammalian Gene Expression by Dynamic Histone Regulations

2020 ◽  
Author(s):  
Deng Tan ◽  
Rui Chen ◽  
Yuejian Mo ◽  
Wei Xu ◽  
Xibin Lu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Expression System ◽  
Transcriptional Activator ◽  
Chromatin Accessibility ◽  
Gene Expressions ◽  
Positive Feedback Loop ◽  
Dynamic Regulation ◽  
Endogenous Gene

AbstractFluctuation (‘noise’) in gene expression is critical for mammalian cellular processes. Numerous mechanisms contribute to its origins, yet large noises induced by single transcriptional activator species remain to be experimentally understood. Here, we combined the dynamic regulation of transcriptional activator binding, histone regulator inhibitors, and single-cell quantification of chromatin accessibility, mRNA, and protein to probe putative mechanisms. Using a light-induced expression system, we show that the transcriptional activator forms a positive feedback loop with histone acetyltransferases CBP/p300. It generates epigenetic bistability in H3K27ac, which contributes to large noise. Disable of the positive feedback loop by CBP/p300 and HDAC4/5 inhibitors also reduces heterogeneity in endogenous genes, suggesting a universal mechanism. We showed that the noise was reduced by pulse-wide modulation of transcriptional activator binding due to alternating the system between high and low monostable states. Our findings could provide a mechanism-based approach to modulate noise in synthetic and endogenous gene expressions.

HSF1 Is a Transcriptional Activator of IL-10 Gene Expression in RAW264.7 Macrophages

Inflammation ◽  
2012 ◽  
Vol 35 (4) ◽  
pp. 1558-1566 ◽  
Author(s):  
Huali Zhang ◽  
Lingli Zhang ◽  
Fengxiu Yu ◽  
Ying Liu ◽  
Qiujuan Liang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcriptional Activator ◽  
Raw264.7 Macrophages

scholarly journals The Temperature-Dependent Expression of the High-Pathogenicity Island Encoding Piscibactin in Vibrionaceae Results From the Combined Effect of the AraC-Like Transcriptional Activator PbtA and Regulatory Factors From the Recipient Genome

2021 ◽  
Vol 12 ◽  
Author(s):  
Marta A. Lages ◽  
Manuel L. Lemos ◽  
Miguel Balado
Keyword(s):  
Gene Expression ◽  
Expression Patterns ◽  
Vibrio Anguillarum ◽  
Transcriptional Activator ◽  
Pathogenicity Island ◽  
Combined Effect ◽  
Temperature Dependent ◽  
Global Regulators ◽  
Relevant Effect ◽  
High Pathogenicity

The high-pathogenicity island irp-HPI is widespread among Vibrionaceae encoding the piscibactin siderophore system. The expression of piscibactin genes in the fish pathogen Vibrio anguillarum is favored by low temperatures. However, information about the regulatory mechanism behind irp-HPI gene expression is scarce. In this work, in-frame deletion mutants of V. anguillarum defective in the putative regulators AraC1 and AraC2, encoded by irp-HPI, and in the global regulators H-NS and ToxRS, were constructed and their effect on irp-HPI gene expression was analyzed at 15 and 25°C. The results proved that only AraC1 (renamed as PbtA) is required for the expression of piscibactin biosynthesis and transport genes. PbtA inactivation led to an inability to grow under iron restriction, a loss of the outer membrane piscibactin transporter FrpA, and a significant decrease in virulence for fish. Inactivation of the global repressor H-NS, which is involved in silencing of horizontally acquired genes, also resulted in a lower transcriptional activity of the frpA promoter. Deletion of toxR-S, however, did not have a relevant effect on the expression of the irp-HPI genes. Therefore, while irp-HPI would not be part of the ToxR regulon, H-NS must exert an indirect effect on piscibactin gene expression. Thus, the temperature-dependent expression of the piscibactin-encoding pathogenicity island described in V. anguillarum is the result of the combined effect of the AraC-like transcriptional activator PbtA, harbored in the island, and other not yet defined regulator(s) encoded by the genome. Furthermore, different expression patterns were detected within different irp-HPI evolutionary lineages, which supports a long-term evolution of the irp-HPI genomic island within Vibrionaceae. The mechanism that modulates piscibactin gene expression could also be involved in global regulation of virulence factors in response to temperature changes.

scholarly journals Glucose- and Glucokinase-Controlled mal Gene Expression in Escherichia coli

2008 ◽  
Vol 191 (3) ◽  
pp. 701-712 ◽  
Author(s):  
Christina Lengsfeld ◽  
Stefan Schönert ◽  
Renate Dippel ◽  
Winfried Boos
Keyword(s):  
Gene Expression ◽  
Escherichia Coli ◽  
Gene Regulation ◽  
Glucose Transporter ◽  
Direct Interaction ◽  
Transcriptional Activator ◽  
Structural Similarity ◽  
Expression In Escherichia Coli ◽  
Maltodextrin Phosphorylase ◽  
Endogenous Induction

ABSTRACTMalT is the central transcriptional activator of allmalgenes inEscherichia coli. Its activity is controlled by the inducer maltotriose. It can be inhibited by the interaction with certain proteins, and its expression can be controlled. We report here a novel aspect ofmalgene regulation: the effect of cytoplasmic glucose and glucokinase (Glk) on the activity and the expression of MalT. Amylomaltase (MalQ) is essential for the metabolism of maltose. It forms maltodextrins and glucose from maltose or maltodextrins. We found that glucose above a concentration of 0.1 mM blocked the activity of the enzyme.malQmutants when grown in the absence of maltodextrins are endogenously induced by maltotriose that is derived from the degradation of glycogen. Therefore, the fact thatglk malQ+mutants showed elevatedmalgene expression finds its explanation in the reduced ability to remove glucose from MalQ-catalyzed maltodextrin formation and is caused by a metabolically induced MalQ−phenotype. However, even in mutants lacking glycogen, Glk controls endogenous induction. We found that overexpressed Glk due to its structural similarity with Mlc, the repressor ofmalT, binds to the glucose transporter (PtsG), releasing Mlc and thus increasingmalTrepression. In addition, even in mutants lacking Mlc (and glycogen), the overexpression ofglkleads to a reduction inmalgene expression. We interpret this repression by a direct interaction of Glk with MalT concomitant with MalT inhibition. This repression was dependent on the presence of either maltodextrin phosphorylase or amylomaltase and led to the inactivation of MalT.

A large internal deletion converts yeast LEU3 to a constitutive transcriptional activator

1989 ◽  
Vol 9 (9) ◽  
pp. 4056-4060
Author(s):  
P Friden ◽  
C Reynolds ◽  
P Schimmel
Keyword(s):  
Gene Expression ◽  
Saccharomyces Cerevisiae ◽  
Amino Acid ◽  
Transcriptional Activator ◽  
Large Block ◽  
Wild Type ◽  
Internal Deletion ◽  
Dense Cluster

LEU3 of Saccharomyces cerevisiae encodes an 886-amino-acid polypeptide that activates transcription of at least five genes by binding to an upstream decanucleotide sequence. This activation is dependent on the inducer alpha-isopropylmalate, the synthesis of which is repressed by leucine. We created a 285-amino-acid LEU3 derivative by removing a large block of internal sequences, including a dense cluster of acidic residues. This deletion protein bound to the decanucleotide sequence in vitro and activated gene expression in vivo. In contrast to wild-type LEU3, the truncated LEU3 protein was an effective transcriptional activator when alpha-isopropylmalate synthesis was repressed by leucine.

scholarly journals SprB Is the Molecular Link between Salmonella Pathogenicity Island 1 (SPI1) and SPI4

2010 ◽  
Vol 192 (9) ◽  
pp. 2459-2462 ◽  
Author(s):  
Supreet Saini ◽  
Christopher V. Rao
Keyword(s):  
Gene Expression ◽  
Transcriptional Activator ◽  
Pathogenicity Island ◽  
Salmonella Pathogenicity Island

ABSTRACT Salmonella pathogenicity island 1 (SPI1) and SPI4 have previously been shown to be jointly regulated. We report that SPI1 and SPI4 gene expression is linked through a transcriptional activator, SprB, encoded within SPI1 and regulated by HilA. SprB directly activates SPI4 gene expression and weakly represses SPI1 gene expression through HilD.

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