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PubMed1998

Repression of the mouse M-lysozyme gene involves both hindrance of enhancer factor binding to the methylated enhancer and histone deacetylation.

In many cases, gene repression mediated by CpG methylation has been demonstrated. Two different mechanisms have been postulated to explain the repressive effect of methylated CpG DNA: establishment of a repressive chromatin configuration and inhibition of DNA binding of transactivating factors. Using the M-lysozyme gene, we analyzed gene expression, CpG demethylation and the in vivo formation of enhancer/protein complexes after inducing demethylation or inhibiting histone deacetylases. We show that trans-cription of a methylated and silent mouse M-lysozyme gene can be induced upon the inhibition of histone deacetylases in the absence of demethylation or in vivo transactivating factor binding to the enhancer. In contrast, DNA demethylation induces both gene activity as well as enhancer complex formation. Therefore, both mechanisms play a role in lysozyme gene repression mediated by methylated DNA: (i) the enhancer cannot be loaded with transacting factors; and (ii) histone deacetylation inhibits transcription.

Acetylation↗
PubMed1997

Activation and repression of the activity of a lead ribozyme by the combination of Pb2+ and Mg2+.

The effect of Pb2+ and Mg2+ on the activity of a lead ribozyme with modified sequences has been studied. At low Pb2+ concentrations, cleavage at a previously reported site (site a) is observed. At higher Pb2+ concentrations, cleavage at a new site (site b) adjacent to site a is observed, while the cleavage at site a is repressed. On the addition of a certain amount of Mg2+, the cleavage at site a is enhanced by almost fourfold, while the cleavage at site b is repressed. Further addition of Mg2+ represses the cleavage at both sites. CD analysis indicates that the structure and stability of the lead ribozyme change depending on the metal conditions. Activation and repression of the activity by the combination of Pb2+ and Mg2+ are rationalized by considering that the two metals compete with each other for binding at two metal-binding sites.

Base Sequence↗
PubMed1977

Are there precursors to repression?

The author examines the possibility that repression has developed out of phylo- and ontogenetic precursors. The adaptive task of repression is to control instinctual behavior by screening out those stimuli (internal or external) which could trigger unacceptable behavior. Habituation, i.e., cessation of response to a repeated stimulis, is a mechanism for controlling behavior, with properties strikingly similar to repression. It operates by inhibiting sensory input, can discriminate and "recognize" the stimuli to be inhibited, and is impaired by brain damage, drugs (especially barbiturates), and perhaps also influenced by hypnosis. The author suggests that repression may be an evolutionary step from habituation, providing for inhibition of irrelevant as well as relevant but undesirable stimuli. In infants, habituation and withdrawal of attention from noxious stimuli operate through similar and perhaps identical mechanisms.

Habituation, Psychophysiologic↗
PubMedDate not supplied

Pervasive emotion recognition deficit common to alexithymia and the repressive coping style.

OBJECTIVE: Previous research has demonstrated a deficit in the ability to recognize emotions in alexithymic individuals. The repressive coping style is thought to preferentially impair the detection of unpleasant compared with pleasant emotions, and the degree of deficit is typically thought to be less severe than in alexithymia. We compared emotion recognition ability in both individuals with alexithymia and those with the repressive coping style. METHODS: Three hundred seventy-nine subjects completed the 20-item Toronto Alexithymia Scale, the Levels of Emotional Awareness Scale, the Marlowe-Crowne Scale (a measure of repressive defensiveness), the Bendig Short Form of the Taylor Manifest Anxiety Scale, and the Perception of Affect Task. The Perception of Affect Task consists of four 35-item emotion recognition subtasks: matching sentences and words, faces and words, sentences and faces, and faces and photographs of scenes. The stimuli in each subtask consist of seven emotions (happiness, sadness, anger, fear, disgust, surprise, and neutral) depicted five times each. Recognition accuracy results were collapsed across subtasks within each emotion category. RESULTS: Highly alexithymic subjects (for all, p<.01) and those with low emotional awareness (for all, p<.001) were consistently less accurate in emotion recognition in all seven categories. Highly defensive subjects (including repressors) were less accurate in the detection of anger, sadness, fear, and happiness (for all, p<.05). Furthermore, scores on the Levels of Emotional Awareness Scale accounted for significantly more variance in performance on the Perception of Affect Task than scores on the Marlowe-Crowne Scale (p<.01). CONCLUSIONS: The results indicate that alexithymia and the repressive coping style are each associated with impairments in the recognition of both pleasant and unpleasant emotions and that the two styles of emotional self-regulation differ more in the magnitude than in the quality of these impairments.

Adaptation, Psychological↗
PubMed1984

Influence of carbon catabolite repression on the G1 arrest of Saccharomyces cerevisiae MATa cells by alpha factor.

Cells of the yeast Saccharomyces cerevisiae of the a mating type were arrested at the G1 phase of the cell division cycle after treatment with alpha factor in a culture medium containing a high concentration (2%, w/v, or higher) of a catabolite-repressing sugar. In media containing either a lower concentration of sugar or a non-fermentable carbon source, the extent of G1 arrest induced by the pheromone was reduced or became undetectable. Under catabolite-derepressing conditions alpha factor was inactivated by a cells at a higher rate than that found in repressing media. These results indicate the existence of a close correlation between the action of alpha factor on a cells and conditions of catabolite repression or derepression. A joint mechanism of action of alpha factor and catabolite-repressing carbon sources on a cells is postulated.

Enzyme Repression↗
PubMed1975

Catabolite repression of Pseudomonas aeruginosa amidase: isolation of promotor mutants.

Among mutants of Pseudomonas aeruginosa isolated from fluoroacetamide medium were some which synthesized amidase at about 5% of the rate of the parent constitutive strain, PAC101. Seven fluoroacetamide-resistant mutants with low amidase activity gave rise to secondary mutant strains on succinate+butyramide plates. One appeared to be an 'up-promotor' mutant and synthesized amidase at a high rate. This mutant, PAC433, was not stimulated by cyclic-AMP and was much less sensitive to catabolite repression by succinate. The mutation conferring resistance to catabolite repression was cotransduced at a frequency of 96% (26/27) with the amidase genes amiR, amiE. Five other revertants had catabolite repression-resistance mutations which were linked to the amidase genes and these also were probably promotor mutants. One strain had a mutation conferring resistance to catabolite repression which was unlinked to the amidase genes.

Acetamides↗
PubMed1976

The effect of nitrogen limitation on catabolite repression of amidase, histidase and urocanase in Pseudomonas aeruginosa.

In Pseudomonas aeruginosa, the synthesis of histidase, urocanase and amidase is severly repressed when succinate is added to a culture growing in pyruvate + ammonium salts medium. When growth is nitrogen-limited, catabolite repression by succinate of histidase and urocanase synthesis does not occur but succinate repression of amidase synthesis persists. Amidase synthesis is not regulated in the same way as histidase synthesis by the availability of other nitrogen compounds for growth. Growth of P. aeruginosa strain PACI in succinate + histidine media is nitrogen-limited since this strain is defective in a histidine transport system. When methyl-ammonium chloride is added to succinate + histidine media, growth inhibition occurs. Mutants isolated from succinate + histidine + methylammonium chloride plates were found to be resistant to catabolite repression by succinate even in ammonium salts media. It is suggested that the hut genes of P. aeruginosa may be regulated in the same way as in Klebsiella aerogenes, by induction by urocanate and activation by either the cyclic AMP-dependent activator protein or by glutamine synthetase.

Amidohydrolases↗
PubMed1993

A lowered concentration of cAMP receptor protein caused by glucose is an important determinant for catabolite repression in Escherichia coli.

A decreased intracellular concentration of cAMP is insufficient to account for catabolite repression in Escherichia coli. We show that glucose lowers the amount of cAMP receptor protein (CRP) in cells. A correlation exists between CRP and beta-galactosidase levels in cells growing under various conditions. Exogenous cAMP completely eliminates catabolite repression in CRP-overproducing cells, while it does not fully reverse the effect of glucose on beta-galactosidase expression in wild-type cells. When the CRP concentration is reduced by manipulating the crp gene, beta-galactosidase expression decreases in proportion to the concentration of CRP. These findings indicate that the lowered concentration of CRP caused by glucose is one of the major factors for catabolite repression. We propose that glucose causes catabolite repression by lowering the intracellular levels of both CRP and cAMP.

Bacterial Proteins↗
PubMed2006

Repressive coping style and autonomic reactions to two experimental stressors in healthy men and women.

Autonomic and affective responses to two different stress tasks were measured in 45 males and 74 females, categorized as repressive, true low-anxious, true high-anxious, and defensive high-anxious. Electrodermal activity (EDA) was used as a measure of sympathetic activity and the high frequency (HF) spectral component of heart rate variability as a measure of parasympathetic activity. Contrary to our predictions, reactivity of repressors did not differ from the reactivity of true low-anxious participants. The results draw attention to previous inconsistent findings within the literature on repressive coping style and autonomic nervous system dysregulation. It is suggested that future research could benefit from the use of more consistent operationalizations of the repressive coping construct and from comparing alternative measures of repressive coping within the same study.

Adaptation, Psychological↗
PubMed1996

The inactivation of hexokinase activity does not prevent glucose repression in Candida utilis.

High hexokinase activity was not related to glucose repression in Candida utilis IGC 3092. The addition of Cibacron Blue 3G-A to growing cells in batch culture led to a permanent in vivo hexokinase inactivation, decreased growth rate and inhibited alcohol dehydrogenase. Hexokinase inactivation up to 90% did not alleviate glucose repression of alpha-glucosidase, as has been described for Saccharomyces cerevisiae and other yeasts. Moreover, when cells were physiologically derepressed by growing them in a chemostat at low glucose concentrations, the highest hexokinase activity was shown by the derepressed cells, and decreased as repression increased. Thus, in our strain of C. utilis, hexokinase activity was inversely proportional to glucose repression.

Candida↗
PubMed2004

Peroxisome proliferator-activated receptor-gamma-independent repression of collagenase gene expression by 2-cyano-3,12-dioxooleana-1,9-dien-28-oic acid and prostaglandin 15-deoxy-delta(12,14) J2: a role for Smad signaling.

Matrix metalloproteinases (MMPs) degrade extracellular matrix components, and overexpression of these enzymes contributes to tissue destruction in arthritis. Of particular importance are the collagenases, MMP-1 and MMP-13, which have high activity against the interstitial collagens in cartilage. In this study, we address the mechanisms of two inhibitors of collagenase gene expression, the synthetic triterpenoid 2-cyano-3,12-dioxooleana-1,9-dien-28-oic acid (CDDO) and 15-deoxy-delta(12,14)-prostaglandin J2 (15-dPGJ2). Although both inhibitors are ligands for the nuclear hormone receptor peroxisome proliferator-activated receptor-gamma (PPAR-gamma), a connection between PPAR-gamma and collagenase gene expression has yet to be established. Here, we test the hypothesis that CDDO and 15-dPGJ2 use PPAR-gamma to repress MMP gene expression. Our findings with the PPAR-gamma antagonist 2-[4-[2-[3-(2,4-difluorophenyl)-1-heptylureido]ethyl]rsqb]-phenylsulfanyl]-2-methylpropionic acid (GW9662) and mouse embryonic fibroblasts lacking PPAR-gamma demonstrate that CDDO and 15-dPGJ2 use PPAR-gamma-independent mechanisms to inhibit collagenase gene expression. To address a potential PPAR-gamma-independent mechanism leading to the repression of MMPs by CDDO, we tested the effect of CDDO on the transforming growth factor-beta (TGF-beta) signaling pathway. We found that CDDO requires Smads (transcription factors activated by TGF-beta) for the repression of MMP-1. Specifically, MMP-1 is inhibited neither by CDDO in the absence of TGF-beta receptor-activated Smad3 nor when a negative regulator, Smad7, attenuates TGF-beta signaling. We conclude that CDDO represses MMP gene expression through a novel PPAR-gamma-independent mechanism that requires Smad signaling.

Animals↗
PubMed1998

Repression of phenol catabolism by organic acids in Ralstonia eutropha.

During batch growth of Ralstonia eutropha (previously named Alcaligenes eutrophus) on phenol in the presence of acetate, acetate was found to be the preferred substrate; this organic acid was rapidly metabolized, and the specific rate of phenol consumption was considerably decreased, although phenol consumption was not abolished. This decrease corresponded to a drop in phenol hydroxylase and catechol-2,3-dioxygenase specific activities, and the synthesis of the latter was repressed at the transcriptional level. Studies with a mutant not able to consume acetate indicated that the organic acid itself triggers the repression. Other organic acids were also found to repress phenol degradation. One of these, benzoate, was found to completely block the catabolism of phenol (diauxic growth). A mutant unable to metabolize benzoate was also unable to develop on benzoate-phenol mixtures, indicating that the organic acid rather than a metabolite involved in benzoate degradation was responsible for the repression observed.

Acetates↗
PubMed1972

Regulation of secondary metabolite biosynthesis: catabolite repression of phenoxazinone synthase and actinomycin formation by glucose.

Synthesis of the secondary metabolite, actinomycin, and the enzyme, phenoxazinone synthase, involved in the biosynthesis of the antibiotic, were shown to be under severe catabolite repression by glucose. Of a variety of hexoses and carbon compounds examined, glucose, and to a lesser extent, mannose, proved to be the most repressive for enzyme synthesis. The repression by glucose was most evident before production of the antibiotic. In a chemically defined medium suitable for actinomycin production, synthesis of phenoxazinone synthase began at the time the glucose (0.1%) supply was depleted. Soon after, antibiotic synthesis was initiated. Galactose, the major carbon source for growth and antibiotic synthesis, was not utilized until the glucose was consumed. Generally, carbon compounds which supported a rapid rate of growth were most effective in producing catabolite repression.

Bacterial Proteins↗
PubMed1972

Mutants of Salmonella typhimurium that are insensitive to catabolite repression of proline degradation.

In Salmonella typhimurium the two enzymes of proline catabolism, proline oxidase and Delta(1)-pyrroline-5-carboxylic acid dehydrogenase, are subject to catabolite repression when the cells are grown in the presence of glucose. Mutants partially relieved of catabolite repression (PutR) for the proline catabolic enzymes have been isolated by selection on agar plates containing glucose and proline. The specificity of the catabolite repression-insensitive character for the enzymes of proline utilization has been confirmed by an analysis of other unrelated catabolic enzymes. Histidase and amylomaltase of the mutant strains are equally as sensitive to glucose repression as are the enzymes from the wild type. All four PutR mutants exhibit higher induced and higher basal levels of proline oxidase as compared with the corresponding wild-type levels. The mutations of three strains tested are cotransducible with constitutive, pleiotrophic-negative and structural gene mutations of the put region. Three-factor crosses indicate that two putR mutations are located at one end of the cluster of put mutations.

Ammonia↗
PubMed1972

Polycistronic effects of catabolite repression on the lac operon.

The catabolite repression caused by glucose and glucose-6-phosphate has been studied for both beta-galactosidase and thiogalactoside transacetylase, the products of the operator proximal and distal cistrons of the lac operon, respectively. We find that both cistrons are affected coordinately by this form of repression. We also find that a single alteration at the lac promoter region is sufficient to abolish sensitivity to repression of both cistrons. From this, we conclude that there is only one target site for catabolite repression in the lac operon.

Acetyltransferases↗
PubMed1973

Involvement of threonine deaminase in repression of the isoleucine-valine and leucine pathways in Saccharomyces cerevisiae.

l-Threonine deaminase (l-threonine dehydratase [deaminating], EC 4.2.2.16) has been shown to be involved in the regulation of three of the enzymes of isoleucine-valine biosynthesis in yeast. Mutations affecting the affinity of the enzyme for isoleucine also affected the repression of acetohydroxyacid synthase, dihydroxyacid dehydrase, and reductoisomerase. The data indicate that isoleucine must be bound for effective repression of these enzymes to take place. In a strain with a nonsense mutation midway in liv 1, the gene for threonine deaminase, starvation for isoleucine or valine did not lead to derepression of the three enzymes; starvation for leucine did. The effect of the nonsense mutation is recessive; it is tentatively concluded, therefore, that intact threonine deaminase is required for derepression by two of the effectors for multivalent repression, but not by the third. A model is presented which proposes that a regulatory species of leu tRNA(leu) is the key intermediate for repression and that threonine deaminase is a positive element, regulating the available pool of charged leu tRNA by binding it.

Culture Media↗
PubMed1973

Induction and repression in the S-adenosylmethionine and methionine biosynthetic systems of Saccharomyces cerevisiae.

Two methionine biosynthetic enzymes and the methionine adenosyltransferase are repressed in Saccharomyces cerevisiae when grown under conditions where the intracellular levels of S-adenosylmethionine are high. The nature of the co-repressor molecule of this repression was investigated by following the intracellular levels of methionine, S-adenosylmethionine, and S-adenosylhomocysteine, as well as enzyme activities, after growth under various conditions. Under all of the conditions found to repress these enzymes, there is an accompanying induction of the S-adenosylmethionine-homocysteine methyltransferase which suggests that this enzyme may play a key role in the regulation of S-adenosylmethionine and methionine balance and synthesis. S-methylmethionine also induces the methyltransferase, but unlike S-adenosylmethionine, it does not repress the methionine adenosyltransferase or other methionine biosynthetic enzymes tested.

Adenosine Triphosphate↗
PubMed1974

Nitrogen repression of the allantoin degradative enzymes in Saccharomyces cerevisiae.

Saccharomyces cerevisiae can utilize allantoin as a sole nitrogen source by degrading it to ammonia, "CO(2)," and glyoxylate. We have previously shown that synthesis of the allantoin degradative enzymes is contingent upon the presence of allophanate, the last intermediate in the pathway. The reported repression of arginase by ammonia prompted us to ascertain whether or not the allantoin degradative system would respond in a similar manner. We observed that the differential rates of allantoinase and allophanate hydrolase synthesis were not decreased appreciably when comparing cultures grown on urea to those grown on urea plus ammonia. These experiments were also performed using the strain and conditions previously reported by Dubois, Grenson, and Wiame. We found allophanate hydrolase production to be twofold repressed by ammonia when that strain was grown on glucose-urea plus ammonia medium. If, however, serine or a number of other readily metabolized amino acids were provided in place of ammonia, production of the allantoin degradative enzymes was quickly (within 20 min) and severely repressed in both strains. We conclude that repression previously attributed to ammonia may result from its metabolism to amino acids and other metabolites.

Alanine↗