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At least 901 records · Page 50Linked to original sources
PubMed2000

Osa-containing Brahma chromatin remodeling complexes are required for the repression of wingless target genes.

The Wingless signaling pathway directs many developmental processes in Drosophila by regulating the expression of specific downstream target genes. We report here that the product of the trithorax group gene osa is required to repress such genes in the absence of the Wingless signal. The Wingless-regulated genes nubbin, Distal-less, and decapentaplegic and a minimal enhancer from the Ultrabithorax gene are misexpressed in osa mutants and repressed by ectopic Osa. Osa-mediated repression occurs downstream of the up-regulation of Armadillo but is sensitive both to the relative levels of activating Armadillo/Pangolin and repressing Groucho/Pangolin complexes present and to the responsiveness of the promoter to Wingless. Osa functions as a component of the Brahma chromatin-remodeling complex; other components of this complex are likewise required to repress Wingless target genes. These results suggest that altering the conformation of chromatin is an important mechanism by which Wingless signaling activates gene expression.

Animals↗
PubMed1990

Metabolic repression of transcription in higher plants.

Using freshly isolated maize mesophyll protoplasts and a transient expression method, I showed that the transcriptional activity of seven maize photosynthetic gene promoters is specifically and coordinately repressed by the photosynthetic end products sucrose and glucose and by the exogenous carbon source acetate. Analysis of deleted, mutated, and hybrid promoters showed that sugars and acetate inhibit the activity of distinct positive upstream regulatory elements without a common consensus. The metabolic repression of photosynthetic genes overrides other forms of regulation, e.g., light, tissue type, and developmental stage. Repression by sugars and repression by acetate are mediated by different mechanisms. The identification of conditions that avoid sugar repression overcomes a major obstacle to the study of photosynthetic gene regulation in higher plants.

Acetates↗
PubMed1992

Cobalamin (vitamin B12) repression of the Cob operon in Salmonella typhimurium requires sequences within the leader and the first translated open reading frame.

Expression of the Cob operon in Salmonella typhimurium is repressed by cobalamin (Cbl). Here it is shown that Cbl repression is mediated by a post-transcriptional regulatory mechanism that requires sequences within the leader and the first translated open reading frame, the cbiA gene. Transcriptional and translational Cob::lacZ fusions containing various lengths of Cob DNA were analysed. In a translational Cob::lacZ fusion 407 bp of leader sequence (+69 to +476) was sufficient to confer normal repression. However in a transcriptional Cob::lacZ fusion a 618 bp region (+69 to +687) was required for normal repression. This 618 bp region included sequences in the leader as well as sequences within the cbiA gene. Point mutations which resulted in loss of repression control were isolated and shown to be clustered in the leader sequence (+257 to +380). This region contains a putative hairpin-loop structure which we propose functions as an RNA operator site for a vitamin B12-responsive repressor protein.

Base Sequence↗
PubMed2004

The histone-like nucleoid structuring protein H-NS represses the Escherichia coli bgl operon downstream of the promoter.

Specificity of repression by the histone-like nucleoid structuring protein and pleiotropic regulator, H-NS, is exceptionally high in case of the Escherichia coli bgl (beta-glucoside) operon. Here we present evidence that H-NS represses the operon at two levels. The binding of H-NS to an upstream silencer results in an approximately threefold repression of the catabolite gene regulator protein (CRP) dependent bgl promoter. In addition, H-NS binds to a silencer region located approximately 600-700 base pairs downstream of the promoter, within the coding region of first gene, bglG, resulting in a approximately sevenfold further decrease of expression. Repression by H-NS at the downstream silencer requires termination factor Rho and is reduced by translation of the bglG mRNA, but is independent of the promoter. This suggests that H-NS induces polarity of transcription by acting as a roadblock to the elongating RNA polymerase. The control of the bgl operon by H-NS at two levels results in a highly specific repression.

Bacterial Proteins↗
PubMed2005

CcpN (YqzB), a novel regulator for CcpA-independent catabolite repression of Bacillus subtilis gluconeogenic genes.

In Bacillus subtilis, the NADPH-dependent glyceraldehyde-3-phosphate dehydrogenase (GapB) and the phosphoenolpyruvate carboxykinase (PckA) enzymes are necessary for efficient gluconeogenesis from Krebs cycle intermediates. gapB and pckA transcription is repressed in the presence of glucose but not via CcpA, the major transcriptional regulator for catabolite repression in B. subtilis. A B. subtilis mini-Tn10 transposant library was screened for clones affected in catabolite repression of gapB. Inactivation of a previously unknown gene, yqzB (renamed ccpN for control catabolite protein of gluconeogenic genes), was found to relieve not only gapB but also pckA transcription from catabolite repression. Purified CcpN specifically bound to the gapB and pckA promoters. ccpN is co-transcribed constitutively with another unknown gene, yqfL. A yqfL deletion lowers the level of gapB and pckA transcription threefold under both glycolytic and gluconeogenic conditions and a ccpN deletion is epistatic over a yqfL deletion. YqfL is thus a positive regulator of the expression of gapB and pckA, the effect of which is not influenced by the metabolic regime of the cell but appears to be mediated by CcpN. ccpN has homologues in many Firmicutes, but not all, while yqfL homologues are widely distributed in Eubacteria and also present in some plants. In all analysed bacterial genomes, ccpN and yqfL are physically linked together or to putative gluconeogenic genes. CcpN thus orchestrates a novel CcpA-independent mechanism for catabolite repression of gluconeogenic genes highly conserved in Firmicutes and appears as a functional analogue of FruR in Enterobacteria. The physiological significance of the regulation mediated via the three B. subtilis global transcription regulators, CcpA, CggR and CcpN, is discussed.

Bacillus subtilis↗
PubMed2005

The CovR response regulator of group A streptococcus (GAS) acts directly to repress its own promoter.

The CovR/S (CsrR/S) two component system is a global regulator of virulence gene expression in the group A streptococcus (GAS, Streptococcus pyogenes). The response regulator, CovR, regulates about 15% of the genes of GAS, including its own operon. Using in vitro DNA binding assays with purified CovR protein, we found that CovR binds a DNA fragment including the covR promoter (Pcov). DNaseI footprint analyses showed that phosphorylation of CovR enhanced and extended the protected regions. The proposed CovR consensus binding sequence (ATTARA) was present at most, but not all protected regions. The effect of replacing the two thymine residues in the consensus binding sequence (CB) with guanine residues was evaluated both in vitro and in vivo. Most, but not all, CB mutations reduced binding of CovR in vitro. Using a transcriptional reporter introduced in single copy into the GAS chromosome, we found that mutations at each CB completely or partially relieved CovR-mediated repression in vivo. This suggests that CovR regulation of Pcov is direct. Further support for this conclusion comes from use of an in vitro GAS transcription system in which CovR was sufficient to mediate repression of Pcov. This repression was enhanced by phosphorylation of the protein. In addition, we found that the CovR binding region overlapping the promoter was essential for wild type repression of Pcov both in vitro and in vivo, suggesting that promoter occlusion is a primary mechanism of Pcov repression by CovR.

Artificial Gene Fusion↗
PubMed2006

Interactions of two abscisic-acid induced WRKY genes in repressing gibberellin signaling in aleurone cells.

Gibberellins (GA) promote while abscisic acid (ABA) inhibits seed germination and post-germination growth. To address the cross-talk of GA and ABA signaling, we studied two rice WRKY genes (OsWRKY51 and OsWRKY71) that are ABA-inducible and GA-repressible in embryos and aleurone cells. Over-expression of these two genes in aleurone cells specifically and synergistically represses induction of the ABA-repressible and GA-inducible Amy32b alpha-amylase promoter reporter construct (Amy32b-GUS) by GA or the GA-inducible transcriptional activator, GAMYB. The physical interactions of OsWRKY71 proteins themselves and that of OsWRKY71 and OsWRKY51 are revealed in the nuclei of aleurone cells using bimolecular fluorescence complementation (BiFC) assays. Although OsWRKY51 itself does not bind to the Amy32b promoter in vitro, it interacts with OsWRKY71 and enhances the binding affinity of OsWRKY71 to W boxes in the Amy32b promoter. The binding activity of OsWRKY71 is abolished by deleting the C-terminus containing the WRKY domain or substituting the key amino acids in the WRKY motif and the zinc finger region. However, two of these non-DNA-binding mutants are still able to repress GA induction by enhancing the binding affinity of the wild-type DNA-binding OsWRKY71 repressors. In contrast, the third non-DNA-binding mutant enhances GA induction of Amy32b-GUS, by interfering with the binding of the wild-type OsWRKY71 or the OsWRKY71/OsWRKY51 repressing complex. These data demonstrate the synergistic interaction of ABA-inducible WRKY genes in regulating GAMYB-mediated GA signaling in aleurone cells, thereby establishing a novel mechanism for ABA and GA signaling cross-talk.

2S Albumins, Plant↗
PubMed1984

Catabolite repression in yeasts is not associated with low levels of cAMP.

relationship between levels of cAMP and catabolite repression in yeasts has been investigated. Strains of Saccharomyces cerevisiae, Schizosaccharomyces pombe and Kluyveromyces fragilis were used. The yeasts were grown on different carbon sources to attain various degrees of repression. Galactose repressed as much as glucose, while maltose was less effective. Full derepression was achieved with ethanol. The enzymes tested were fructose-bisphosphatase, malate dehydrogenase, glutamate dehydrogenase (NAD dependent), cytochrome oxidase and isocitrate lyase (this last enzyme was found to be absent in Schizosaccharomyces). The levels of cAMP were 2-3 times higher in the repressed conditions than in the derepressed ones. It is therefore concluded that in yeasts catabolite repression is not mediated by a lowering of the intracellular concentration of cAMP.

Cyclic AMP↗
PubMed1989

Repression of cytochrome P-450c gene expression by cotransfection with adenovirus E1a DNA.

Gene expression of rat cytochrome P-450c (P-450c) depends upon inducible enhancers scattered in the 5'-upstream region of the gene. We show that expression of the P-450c gene is repressed by contransfection with adenovirus E1a DNA, regardless of the presence or absence of inducers, in a transient expression system of HeLa cells. Since cotransfection of either 13S or 12S E1a cDNA was effective in the repression, the region necessary for repression could be separated from that of transactivation of other adenovirus early genes. Moreover, we investigated the regions responsible for the inhibitory activity using in-frame deletion mutants lacking internal or external portions of the E1a proteins. The sequence responsible for the repression was located in the amino-terminal half of the E1a proteins. The inducible expression of the chimeric plasmid containing a 24-base-pair enhancer sequence of the P-450c gene placed in a heterologous promoter of SV40 was repressed by cotransfection with E1a DNA, suggesting strongly that the inhibitory effect of the E1a proteins upon P-450c gene expression was caused by blocking the enhancer activity.

Adenoviridae↗
PubMed1997

1alpha,25-dihydroxyvitamin D3 and a variety of its natural metabolites transcriptionally repress nuclear-factor-kappaB-mediated interleukin-8 gene expression.

Regulation of interleukin-8 (IL-8) gene transcription occurs mainly through the sequences -94 to -71 of the 5'-flanking region of the IL-8 gene, involving the transcription factors nuclear factor for interleukin-6 (NF-IL-6) and nuclear factor kappaB (NF-kappaB). The human melanoma cell line A3 was derived from G-361 cells by stable transfection with an IL-8 promoter-luciferase construct containing these sequences. 1alpha,25-Dihydroxyvitamin D3 (calcitriol) repressed IL-8 promoter activity induced by tumor necrosis factor-alpha (TNF-alpha) by 50%, compared to 30% inhibition using dexamethasone, an effect consistent with its effect on TNF-alpha-induced IL-8 release and IL-8 mRNA levels. A variety of vitamin D metabolites caused the same repressive effect on IL-8 promoter activation as calcitriol. However, only those metabolites which were able to transactivate a classical vitamin D response element had the ability to repress IL-8 promoter activation, suggesting that this repression is mediated via vitamin D receptor (VDR). Furthermore, overexpression of VDR in the parental G-361 cell line enhanced the repressive effect of calcitriol on activation of the IL-8 promoter by either TNF-alpha stimulation or overexpression of the NF-kappaB subunit p65. Electrophoretic mobility shift assays using nuclear extracts from A3 cells showed that calcitriol decreased the abundance of nuclear factors bound to the NF-kappaB binding site of the IL-8 promoter and this reduced binding of NF-kappaB proteins presumably contributes to its inhibitory action.

Binding Sites↗
PubMed1997

Influence of mutations in hexose-transporter genes on glucose repression in Kluyveromyces lactis.

The variability of Kluyveromyces lactis strains in sensitivity to glucose is correlated with genetic differences in Kluyveromyces hexose transporter (KHT) genes. The glucose sensitive strain JA6 was shown to contain an additional gene, KHT2, not found in strains that are less sensitive. KHT2 is tandemly arranged with KHT1 which is identical to the low-affinity transporter gene RAG1, except for the C-terminus. Sequence analysis indicated that most of KHT2 had been lost by a recombination event between KHT1 and KHT2 generating the chimeric gene RAG1. Recombination between KHT1 and KHT2 was also found in mutants of JA6 selected as 2-deoxyglucose resistant colonies. These mutants, like kht1 kht2 double mutants were unable to grow on glucose when respiration was blocked (Rag- phenotype) and glucose repression was strongly reduced. kht1 or kht2 single mutants of JA6 were Rag+ but still an influence of the kht mutations on glucose repression was detectable. Repression was not affected in a Rag- mutant deleted for the phosphoglucose isomerase gene suggesting that the influence of transporter genes on repression is not caused by a reduction of the glycolytic flux. The data rather suggest that sensitivity to glucose repression is dependent on the rate of glucose uptake.

Amino Acid Sequence↗
PubMed2004

Repression of Pseudomonas putida phenanthrene-degrading activity by plant root extracts and exudates.

The phenanthrene-degrading activity (PDA) of Pseudomonas putida ATCC 17484 was repressed after incubation with plant root extracts of oat (Avena sativa), osage orange (Maclura pomifera), hybrid willow (Salix alba x matsudana), kou (Cordia subcordata) and milo (Thespesia populnea) and plant root exudates of oat (Avena sativa) and hybrid poplar (Populus deltoides x nigra DN34). Total organic carbon content of root extracts ranged from 103 to 395 mg l(-1). Characterization of root extracts identified acetate (not detectable to 8.0 mg l(-1)), amino acids (1.7-17.3 mg l(-1)) and glucose (1.6-14.0 mg l(-1)), indicating a complex mixture of substrates. Repression was also observed after exposure to potential root-derived substrates, including organic acids, glucose (carbohydrate) and glutamate (amino acid). Carbon source regulation (e.g. catabolite repression) was apparently responsible for the observed repression of P. putida PDA by root extracts. However, we showed that P. putida grows on root extracts and exudates as sole carbon and energy sources. Enhanced growth on root products may compensate for partial repression, because larger microbial populations are conducive to faster degradation rates. This would explain the commonly reported increase in phenanthrene removal in the rhizosphere.

Acetates↗
PubMed2006

Evidence for ORC-dependent repression of budding yeast genes induced by starvation and other stresses.

The highly conserved origin recognition complex (ORC) is required for repressing genes in the silent mating type loci of budding yeast. Here we report that at a non-permissive temperature, the temperature-sensitive orc2-1 mutation induces the expression of more than 500 genes, the majority of which are also induced during starvation of wild-type cells. Many genes induced by starvation or by the orc2-1 mutation are also induced by inactivation of proteins required for chromatin-mediated repression of transcription. Genes induced by the orc2-1 mutation, starvation, or inactivation of repressor proteins, map near ORC-binding loci significantly more frequently compared to all genes. Genes repressed by starvation map near ORC-binding sites less frequently compared to all genes, which suggests they have been evolutionarily excluded from regions of repressive chromatin near ORC-binding sites. Deletion of sequences containing ORC-binding sites near the DAL2 and DAL4 genes in the DAL gene cluster, which are induced by either the orc2-1 mutation or by starvation, constitutively activates these genes and abolishes their activation by the orc2-1 mutation. Our findings suggest a role for ORC in the repression of a large number of budding yeast genes induced by starvation or other aspects of a deleterious environment.

Apoptosis↗
PubMed1996

Cyclic AMP-independent catabolite repression in bacteria.

Until recently, only one mechanism of catabolite repression in bacteria, a mechanism dependent on the cyclic AMP receptor protein of Escherichia coli, was understood in molecular detail. Two cyclic AMP-independent catabolite repression mechanisms are currently under study. One such mechanism, found in E. coli, involves the catabolite repressor/activator (Cra) protein (formerly designated the fructose repressor FruR) which represses sugar catabolic systems and activates sugar anabolic systems. When catabolites bind to Cra, Cra dissociates from the DNA causing catabolite activation and catabolite repression, respectively. The second such mechanism, found in Bacillus subtilis, involves a catabolite-activated, ATP-dependent protein kinase that phosphorylates a specific seryl residue in the small phosphocarrier protein, HPr, of the phosphotransferase system. HPr(ser-P) binds to a transcription factor, CcpA, to promote DNA binding. DNA binding of the complex in turn promotes catabolite repression or catabolite activation, depending on the target operon. The characterization of these novel mechanisms establishes that cyclic AMP-independent catabolite control is operative in bacteria, and that multiple mechanisms of catabolite control evolved independently of each other.

Bacillus subtilis↗
PubMed1997

Carbon repression in Aspergilli.

Many microorganisms prefer easily metabolizable carbon sources over alternative, less readily metabolized carbon sources. One of the mechanisms to achieve this is repression of the synthesis of enzymes related to catabolism of the alternative carbon sources, i.e. carbon repression. It is now clear that in Aspergillus nidulans and Aspergillus niger the repressor protein CREA plays a major role in carbon repression. CREA inhibits transcription of many target genes by binding to specific sequences in the promoter of these genes. Unfortunately there is little information on other components of the signalling pathway that triggers repression by CREA. In this review we summarize the current understanding of carbon repression in Aspergilli.

Aspergillus↗
PubMed1993

Position-effect variegation and z1 mediated white repression in the In(1)wis system in Drosophila melanogaster.

We have characterized a new X-chromosomal inversion in Drosophila melanogaster, extending from just distal of white to just proximal of the bb locus. The inversion places the w-isoxanthopterinless (wis) allele close to heterochromatin and under the influence of position-effect variegation (PEV). The wis gene activity is also regulated by chromosome pairing-dependent z1-mediated repression. By changing the environment, using specific second site modifiers, altering the amount of heterochromatin, and disturbing the chromosome pairing, we have been able to separately affect the two regulatory phenomena and analyse their respective impact on the wis regulation. We provide evidence that under normal conditions PEV and z1 mediated white repression are additive. However, at extreme levels of wis repression by PEV, changes in the z1-mediated interactions are not observable. This indicates that PEV is epistatic to z1-mediated regulation of wis. We also show that deficiencies in the short arm of Y act as suppressors of the z1-mediated white repression. This suppression does not influence PEV and is thus not due to the lower amount of heterochromatin. We propose that nonhomologous chromosome pairing between X and Y is important for the synapsis-dependent z1-mediated repression of white transcription activity in this system.

Animals↗
PubMed1989

Rhizobacteria of cotton and their repression of seedling disease pathogens.

During the 1983 field season, the rhizobacteria (including organisms from rhizosphere soil and the root rhizoplane) of cotton plants at one location in Mississippi were inventoried at different plant growth stages. Isolates (1,000) were identified to the genus level and characterized for repression of Pythium ultimum and Rhizoctonia solani. Cotton seedlings were initially colonized by bacteria of many different genera, and populations quickly reached 10 CFU/g of root tissue. As the season progressed, the bacterial populations declined as root mass increased and the roots became more woodlike in consistency. Fluorescent pseudomonads were the most numerous gram-negative rhizobacterial isolates of those that were randomly collected and identified, and they provided the largest number of isolates with fungal repressive activity. Several other gram-negative bacterial genera were recovered throughout the growing season, and some gram-positive bacteria were also isolated routinely, but at lower numbers. There was no correlation between the proportion of rhizobacterial isolates that possessed fungal repressive activity and the plant growth stage from which the isolates were obtained. Approximately twice as many bacterial isolates demonstrated fungal repression in the agar assay compared with the inplanta assay, and isolates were found more frequently with fungal repressive activity against P. ultimum than against R. solai.

Journal Article↗
PubMed1988

High-affinity glucose transport in Saccharomyces cerevisiae is under general glucose repression control.

Saccharomyces cerevisiae mutants defective in growth on low glucose concentration (lgn mutants) were isolated and screened for abnormal glucose transport. Nine complementation groups were identified, falling into two broad groups: those unable to significantly derepress high-affinity (low-Km) glucose uptake (lgn1, lgn4, lgn5, lgn7, and lgn8), and those with elevated repressed levels of high-affinity uptake that either derepress to normal or near normal levels of high-affinity uptake with loss of low-affinity transport (lgn2 and lgn3) or derepress only slightly, appearing to have an intermediate yet constitutive level of high-affinity transport (lgn6 and lgn9). Further analysis of the lgn mutations revealed pleiotropic phenotypes most consistent with the true defect being in regulation or expression of glucose repression and derepression. The kinetics of glucose uptake in strains carrying known mutations preventing derepression of glucose-repressible functions (snf1, snf2, snf4, and snf6) demonstrated that three of these mutations (snf1, snf4, and snf6) were similarly defective in derepression of high-affinity glucose uptake. The snf2 and snf5 mutations had no apparent effect on glucose uptake. Two mutations resulting in constitutive expression of glucose-repressible functions, cid1 and reg1, resulted in constitutive expression of high-affinity glucose uptake. These data support the conclusion that high-affinity glucose uptake in Saccharomyces cerevisiae is under general glucose repression control. The implications of other properties of these mutants are discussed.

Biological Transport↗