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PubMed1999

Glucose repression of the Kluyveromyces lactis invertase gene KlINV1 does not require Mig1p.

Kluyveromyces lactis, a budding yeast related to Saccharomyces cerevisiae, can grow on a wider variety of substrates and shows less sensitivity to glucose repression than does Saccharomyces cerevisiae. Many genes that are subject to glucose repression in S. cerevisiae are repressed only weakly or not at all in K. lactis. The molecular basis for this difference is largely unknown. To compare the mechanisms that regulate glucose repression in K. lactis and S. cerevisiae, we decided to clone and analyse an invertase gene from K. lactis. The SUC2 gene, which encodes invertase in S. cerevisiae, is strongly regulated by glucose and serves as a model system for studies on glucose repression. The invertase gene of K. lactis, KlINV1, was isolated by colony hybridization using a conserved region within the inulinase gene of K. marxianus as a probe. Two independent clones obtained were shown to contain the same ORF of 1827 bp. The deduced amino acid sequence is 59% similar to that of the K. marxianus inulinase and shows 49% similarity to ScSuc2p. Gene disruption experiments and low-stringency Southern analysis indicate that KlINV1 is a unique gene in K. lactis. Northern analysis revealed that the transcription of KlINV1 is strongly repressed in the presence of glucose, but, in contrast to the case in S. cerevisiae, repression is independent of KlMig1p.

Amino Acid Sequence↗
PubMed1986

Transcription of the speC (ornithine decarboxylase) gene of Escherichia coli is repressed by cyclic AMP and its receptor protein.

The speC gene encoding ornithine decarboxylase (ODC) in Escherichia coli is negatively regulated by cAMP and the cAMP receptor protein (CRP). In minicells transformed with the plasmid pODC bearing speC, cAMP supplementation repressed ODC synthesis. In a cell-free protein synthesizing system directed by pODC, cAMP at 10(-5) M repressed ODC synthesis by 90%. This repression required a functional CRP as cAMP failed to repress ODC synthesis in vitro in an extract prepared from a crp- strain; the addition of purified CRP to the crp- extract restored the ability of cAMP to repress ODC synthesis. In a prototroph transformed with the plasmid pCOD bearing a speC::tet chimeric gene, cAMP supplementation decreased tetracycline (Tc) resistance. In contrast, in crp- strains transformed with pCOD or pTET (TcR), cAMP supplementation did not change their Tc resistance. When a cya- strain was supplemented with 2 mM cAMP, steady state levels of ODC mRNA were repressed by 80%. However, when a isogenic crp- strain was supplemented with 2 mM cAMP, no repression of ODC mRNA was observed. These results indicate that the cAMP-CRP complex exerts negative transcriptional control of ODC synthesis as a function of the speC promoter.

Cyclic AMP↗
PubMed1997

A sucrose repression element in the Phaseolus vulgaris rbcS2 gene promoter resembles elements responsible for sugar stimulation of plant and mammalian genes.

Protoplasts isolated from the primary leaves of Phaseolus vulgaris L. were used in transient expression experiments to identify promoter sequences of the P. vulgaris rbcS2 gene, encoding ribulose 1,5-bisphosphate carboxylase/oxygenase small subunit, concerned with sucrose repression. The protoplasts supported high rates of expression of the chloramphenicol acetyl transferase reporter gene fused to 1433 bp of the rbcS2 5' flanking sequences. Expression was repressed by 50 mM sucrose whereas that driven by control promoters was not. Assays of promoter deletions revealed that 203 bp 5' to the transcription start site were sufficient for high rates of sucrose-repressible expression. A -187 bp deletion supported much lower rates of expression and was not subject to sucrose repression. The -203 to -187 bp region contains sequences resembling elements involved in the sugar stimulation of transcription of other genes: the SURE (sucrose response element) of plant genes and the ChoRE (carbohydrate response element) of mammalian genes. A G-box (CACGTG) located at -200 to -205 was important for high levels of sucrose-repressible expression, since deletion of a nucleotide from this element in the context of the 1433 bp promoter gave much reduced expression. However, a modified G-box (CcCGTG) in the -203 bp fusion and adjacent vector sequences remained functional. Measurements of rbcS and chalcone synthase (CHS) transcript levels in the protoplasts indicated that 4 mM sucrose was sufficient to repress or stimulate the respective genes. Further experiments suggested that metabolism of 6-carbon sugars is the signal for rbcS repression and CHS stimulation.

Acyltransferases↗
PubMed1990

Site-directed mutagenesis of a catabolite repression operator sequence in Bacillus subtilis.

Catabolite repression of the Bacillus subtilis alpha-amylase gene (amyE) involves an operator sequence located just downstream of the promoter (amyR), overlapping the transcription start site. Oligonucleotide site-directed mutagenesis of this sequence identified bases required for catabolite repression. Two mutations increased both the 2-fold symmetry of the operator and the repression ratio. Although many mutations reduced the repression ratio 3- to 11-fold, some also caused a 2-fold or greater increase in amylase production. Others caused hyperproduction without affecting catabolite repression. Homologous sequences in other catabolite-repressed B. subtilis promoters suggest a common regulatory site may be involved in catabolite repression.

Bacillus subtilis↗
PubMed1996

Repression of a matrix metalloprotease gene by E1A correlates with its ability to bind to cell type-specific transcription factor AP-2.

Adenovirus E1A 243-amino acid protein can repress a variety of enhancer -linked viral and cellular promoters. This repression is presumed to be mediated by its interaction with and sequestration of p3OO, a transcriptional coactivator. Type IV 72-kDa collagenase is one of the matrix metalloproteases that has been implicated in differentiation, development, angiogenesis, and tumor metastasis. We show here that the cell type-specific transcription factor AP-2 is an important transcription factor for the activation of the type IV 72-kDa collagenase promoter and that adenovirus E1A 243-amino acid protein represses this promoter by targeting AP-2. Glutathione S-transferase-affinity chromatography studies show that the E1A protein interacts with the DNA binding/dimerization region of AP-2 and that the N-terminal amino acids of E1A protein are required for this interaction. Further, E1A deletion mutants which do not bind to p3OO can repress this collagenase promoter as efficiently as the wildtype E1A protein. Because the AP-2 element is present in a variety of viral and cellular enhancers which are repressed by E1A, these studies suggest that E1A protein can repress cellular and viral promoter/enhancers by forming a complex with cellular transcription factors and that this repression mechanism may be independent of its interaction with p3OO.

Adenovirus E1A Proteins↗
PubMed1994

Recovered-memory therapy and robust repression: influence and pseudomemories.

A subset of the psychotherapists practicing trauma-focused therapy predicate their treatment on the existence of a newly claimed, powerful form of repression that differs from repression as used in the psychoanalytic tradition and from amnesia in any of its recognized forms. Recovered-memory specialists assist patients to supposedly retrieve vast quantities of information (e.g., utterly new dramatic life histories) that were allegedly unavailable to consciousness for years or decades. We refer to the hypothesized mental mechanism as "robust repression" and call attention to the absence of evidence documenting its validity and to the differences between it and other mental mechanisms and memory features. No recovered-memory practitioner has ever published a full specification of the attributes of this mechanism. That is, the properties it would have to have for the narratives developed during therapy to be historically accurate to any significant degree. This article reports a specification of the properties of the robust repression mechanism based on interviews with current and former patients, practitioners' writings, and reports to researchers and clinicians. The spread of reliance on the robust repression mechanism over the past 20 years through portions of the clinical community is traced. While involved in therapy, patients of recovered-memory practitioners come to believe that they have either instantly repressed large numbers of discrete events or simultaneously repressed all information about abuse they may have endured for as long as a decade.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1978

Transient repression of beta-galactosidase synthesis by glucose-6-phosphate in a mutant of Escherichia coli lacking enzyme II specific for glucose in the phosphoenolpyruvate-sugar phosphotransferase system.

The effects of glucose and glucose-6-phosphate in initiating the repression of beta-galactosidase synthesis were studied using a mutant of Escherichia coli K12 which lacks glucose-specific enzyme II of the phosphoenolpyruvate-sugar phosphotransferase system. It was found that glucose-6-phosphate causes transient repression of beta-galactosidase synthesis but glucose does not cause transient repression in this mutant. Evidence was obtained that both the presence of an active transport system for glucose-6-phosphate in the cells and glucose-6-phosphate in the medium are necessary for the initiation of transient repression. No metabolism of glucose-6-phosphate is required. Upon depletion of glucose-6-phosphate in the medium the transient repression was reversed. After the reversal the rate of enzyme synthesis was high in the cells which had been exposed to a high concentration of glucose-6-phosphate. It was concluded that the translocation of glucose-6-phosphate across the membranes is the primary event which affects both the initiation of and the recovery from the transient repression. During the transient repression the cellular content of cyclic adenosine 3',5'-monophosphate decreased significantly.

Biological Transport, Active↗
PubMedDate not supplied

Repressive coping style, acute stress disorder, and posttraumatic stress disorder after myocardial infarction.

OBJECTIVE: The study examined the associations between repressive coping style, acute stress disorder (ASD) and subsequent posttraumatic stress disorder (PTSD) after myocardial infarction (MI) to ascertain the efficacy of repressive coping style in immediate and long-term adjustment to stress. METHODS: A total of 116 MI patients were examined twice: within a week of their MI (time 1) and 7 months later (time 2). At time 1, repressive coping style, perceived threat, and ASD were measured by self-report questionnaires. In addition, medical measures indicative of the severity of the MI were obtained from patients' hospital records. At time 2, PTSD was assessed. The distribution of the repressive coping style was compared with that of 72 matched control subjects. RESULTS: Findings revealed the adaptiveness of repressive coping style both in the immediate and longer-term aftermath of MI: repressors endorsed less ASD and PTSD than nonrepressors. In addition, the contribution of repressive coping style to PTSD was unique and beyond the implications of severity of MI, perceived threat, and immediate ASD. CONCLUSIONS: The findings support the role of repressive coping style as a stress-buffer; several mechanisms that explain this role are suggested.

Adaptation, Psychological↗
PubMed1993

The glucose-6-phosphate-isomerase reaction is essential for normal glucose repression in Saccharomyces cerevisiae.

Wild-type Saccharomyces cerevisiae and a strain carrying a deletion in the glucose-6-phosphate-isomerase gene (pgi1) were grown in carbon-limited continuous cultures on a mixture of fructose and galactose. Pulses of glucose, fructose and galactose were given to these cultures to investigate whether the pgi1 strain was capable of normal glucose repression. Glucose and galactose pulses inhibited fructose consumption and thus glycolysis in the pgi1 strain by a combination of competition between glucose and fructose at the uptake and/or phosphorylation level and inhibition of fructose uptake and/or phosphorylation by glucose 6-phosphate. Fructose pulses administered to the pgi1 strain transiently decreased the glycolytic flux downstream of fructose-1,6-bisphosphate. Transcriptional induction of the PDC1 gene (encoding pyruvate decarboxylase) was observed after glucose or galactose pulses were applied to the pgi1 strain, demonstrating that metabolism of these sugars beyond glucose 6-phosphate is dispensable for PDC1 induction. Fructose also induced PDC1 transcription, indicating that intracellular sugars could act as trigger for PDC1 induction or, alternatively, that two inductors are present. In contrast to the wild-type transcriptional inhibition of the glucose-repressible genes, HXK1 and GAL10 (encoding hexokinase isoenzyme 1 and uridine diphosphoglucose-4-epimerase, respectively) did not occur upon addition of glucose or fructose to the pgi1 mutant. Transcriptional repression was observed after application of the fructose pulse when the yeast had resumed metabolism of fructose. These results demonstrate that the initial signal for catabolite repression is not generated by high sugar concentrations or high concentrations of intermediates; moreover a simple role for the hexokinases can also be excluded. The absence of an increased glycolytic flux in the pgi1 mutant after administration of the sugar pulses while the concentrations of sugar and glycolytic intermediates were high, suggests that the initial signal for glucose repression could be linked to an increased glycolytic flux. The occurrence of PDC1 induction in the pgi1 strain while GAL10/HXKI repression is absent, demonstrates that the initial signals for catabolite induction and catabolite repression are different.

Blotting, Northern↗
PubMed1971

Methionine-mediated repression in Saccharomyces cerevisiae: a pleiotropic regulatory system involving methionyl transfer ribonucleic acid and the product of gene eth2.

Detailed study of methionine-mediated repression of enzymes involved in methionine biosynthesis in Saccharomyces cerevisiae led to classification of these enzymes into two distinct regulatory groups. Group I comprises four enzymes specifically involved in different parts of methionine biosynthesis, namely, homoserine-O-transacetylase, homocysteine synthetase, adenosine triphosphate sulfurylase, and sulfite reductase. Repressibility of these enzymes is greatly decreased in strains carrying a genetically impaired methionyl-transfer ribonucleic acid (tRNA) synthetase (mutation ts(-) 296). Conditions leading to absence of repression in the mutant strain have been correlated with a sharp decrease in bulk tRNA(met) charging, whereas conditions which restore repressibility of group I enzymes also restore tRNA(met) charging. These findings implicate methionyl-tRNA in the regulatory process. However, the absence of a correlation in the wild type between methionyl-tRNA charging and the levels of methionine group I enzymes suggests that only a minor iso accepting species of tRNA(met) may be devoted with a regulatory function. Repressibility of the same four enzymes (group I) was also decreased in strains carrying the regulatory mutation eth2(r). Although structural genes coding for two of these enzymes, as well as mutations ts(-) 296 and eth2(r) segregate independently to each other, synthesis of group I enzymes is coordinated. The pleiotropic regulatory system involved seems then to comprise beside a "regulatory methionyl tRNA(met)," another element, product of gene eth2, which might correspond either to an aporepressor protein or to the "regulatory tRNA(met)" itself. Regulation of group II enzymes is defined by response to exogenous methionine, absence of response to either mutations ts(-) 296 and eth2(r), and absence of coordinacy with group I enzymes. However, the two enzymes which belong to this group and are both involved in threonine and methionine biosynthesis undergo distinct regulatory patterns. One, aspartokinase, is subject to a bivalent repression exerted by threonine and methionine, and the other, homoserine dehydrogenase, is subject only to methionine-mediated repression. Participation of at least another aporepressor and another corepressor, different from the ones involved in regulation of group I enzymes, is discussed.

Acyltransferases↗
PubMed1971

Repression of aromatic amino acid biosynthesis in Escherichia coli K-12.

Mutants of Escherichia coli K-12 were isolated in which the synthesis of the following, normally repressible enzymes of aromatic biosynthesis was constitutive: 3-deoxy-d-arabinoheptulosonic acid 7-phosphate (DAHP) synthetases (phe and tyr), chorismate mutase T-prephenate dehydrogenase, and transaminase A. In the wild type, DAHP synthetase (phe) was multivalently repressed by phenylalanine plus tryptophan, whereas DAHP synthetase (tyr), chorismate mutase T-prephenate dehydrogenase, and transaminase A were repressed by tyrosine. DAHP synthetase (tyr) and chorismate mutase T-prephenate dehydrogenase were also repressed by phenylalanine in high concentration (10(-3)m). Besides the constitutive synthesis of DAHP synthetase (phe), the mutants had the same phenotype as strains mutated in the tyrosine regulatory gene tyrR. The mutations causing this phenotype were cotransducible with trpA, trpE, cysB, and pyrF and mapped in the same region as tyrR at approximately 26 min on the chromosome. It is concluded that these mutations may be alleles of the tyrR gene and that synthesis of the enzymes listed above is controlled by this gene. Chorismate mutase P and prephenate dehydratase activities which are carried on a single protein were repressed by phenylalanine alone and were not controlled by tyrR. Formation of this protein is presumed to be controlled by a separate, unknown regulator gene. The heat-stable phenylalanine transaminase and two enzymes of the common aromatic pathway, 5-dehydroquinate synthetase and 5-dehydroquinase, were not repressible under the conditions studied and were not affected by tyrR. DAHP synthetase (trp) and tryptophan synthetase were repressed by tryptophan and have previously been shown to be under the control of the trpR regulatory gene. These enzymes also were unaffected by tyrR.

Aldehyde-Lyases↗
PubMed1989

cis sequences involved in modulating expression of Bacillus licheniformis amyL in Bacillus subtilis: effect of sporulation mutations and catabolite repression resistance mutations on expression.

Nutrient conditions which trigger sporulation also activate expression of the Bacillus licheniformis alpha-amylase gene, amyL. Glucose represses both spore formation and expression of amyL. A fusion was constructed between the B. licheniformis alpha-amylase regulatory and 5' upstream sequences (amyRi) and the Escherichia coli lacZ structural gene to identify sequences involved in mediating temporal activation and catabolite repression of the amyL gene in Bacillus subtilis. amyRi-directed expression in a variety of genetic backgrounds and under different growth conditions was investigated. A 108-base-pair sequence containing an inverted repeat sequence, ribosome-binding site, and 26 codons of the structural gene was sufficient to mediate catabolite repression of amyL. spo0 mutations (spo0A, spo0B, spo0E, and spo0H) had no significant effect on temporal activation of the gene fusion when the recipient strains were grown in nonrepressing medium. However, in glucose-grown cultures the presence of a spo0A mutation resulted in more severe repression of amyRi-lacZ. In contrast, a spo0H mutation reduced the repressive effect of glucose on amyRi-lacZ expression. The spo0A effect was relieved by an abrB mutation. Initiation of sporulation is not a prerequisite for either temporal activation or derepression of alpha-amylase synthesis. Mutations causing resistance to catabolite repression in B. subtilis GLU-47, SF33, WLN30, and WLN104 also relieved catabolite repression of amyRi-lacZ.

Bacillus↗
PubMed1994

Catabolite repression of the Bacillus subtilis hut operon requires a cis-acting site located downstream of the transcription initiation site.

Expression of the Bacillus subtilis hut operon is subject to regulation by catabolite repression. A set of hut-lacZ transcriptional fusions was constructed and used to identify two cis-acting sites involved in catabolite repression. The hutOCR1 operator site lies immediately downstream of the hut promoter and weakly regulates hut expression in response to catabolite repression. The downstream hutOCR2 operator site lies within the hutP gene, between positions +203 and +216, and is required for wild-type levels of catabolite repression. Both the hutOCR1 and hutOCR2 operators have sequence similarity to the sites which mediate catabolite repression of several other B. subtilis genes. Two mutations which relieve catabolite repression of hut expression were found to alter the nucleotide sequence of the hutOCR2 operator. Catabolite repression of hut expression was partially relieved in strains containing the ccpA mutation but not in strains containing either the pai or hpr mutation.

Aldose-Ketose Isomerases↗
PubMed1967

Catabolite repression and pyruvate metabolism in Escherichia coli.

A study was made of the reactions involved in the cellular regulatory function known as catabolite repression. These studies employed the glucose-repressible, beta-galactosidase system of Escherichia coli and involved an investigation of glucose dissimilation under cultural conditions capable of permitting or preventing expression of catabolite repression. The results indicated that reactions associated with pyruvate decarboxylation are of particular importance in influencing repression. This conclusion was based on results obtained by measurement of differential rates of C(14)O(2) evolution from specifically labeled (14)C-glucose substrates, and by measurements of H(2) evolution during anaerobic growth. Catabolite repression measured in relation to steady-state growth rates indicated that the repression mechanism may in fact be a direct consequence of a cell's energy balance, as dictated by the production from pyruvate of "high-energy" molecules such as adenosine triphosphate or acetyl-coenzyme A. The apparent involvement of pyruvate metabolism in both the energetics and the expression of catabolite repression in E. coli is consistent with this view.

Carbon Isotopes↗
PubMed1969

Corepressor system for catabolite repression of the lac operon in Escherichia coli.

Acetylated amino sugars, normally used in the biosynthesis of cell walls and cell membranes, were found to play a role as corepressors for catabolite repression of the lac operon in Escherichia coli. This conclusion was derived from studies conducted on mutants of E. coli that were able to assimilate an exogenous source of N-acetylglucosamine (AcGN) but were unable to dissimilate or grow on this compound. At concentrations less than 10(-4)m, AcGN caused severe catabolite repression of beta-galactosidase synthesis in cultures grown under either nonrepressed or partially repressed conditions. This repression occurred in the absence of any effect of AcGN on either the carbon and energy metabolism or the growth of the organism. In addition, this repression by AcGN occurred in a mutant strain that is constitutive for beta-galactosidase production, demonstrating that the AcGN effect does not involve the uptake of inducer. This model for the corepressor system of catabolite repression is discussed in relation to the existing theories on repression of the lac operon.

Carbon Isotopes↗
PubMed1984

Repression theory: a new look at the cornerstone.

The purpose of this paper is to revise the theory of repression so as to resolve long-standing theoretical inconsistencies, to increase congruence with data and concepts generated by new clinical problems; and to contribute to analysts' understanding of patients. Our approach is based on Freud's conception of psychic structure as based on representations, which stem from needs mediated through satisfying experiences. We have also adhered to Freud's persistently held ideas of primal repression as a state with its roots in trauma, and of repression proper as a defensive process evolving out of primal repression. The most significant clinical findings are the possibility of primal repression at any stage of life, not just in childhood; and the possibility of healthy development without repression. The revised theory leads to a new general classification of analysands and clarifies the need for both components of the psychoanalytic method, resolving intrapsychic conflicts and facilitating emotional maturation. The most significant theoretical outcome is a reaffirmation of repression as the basis for any general theory of psychopathology.

Adolescent↗
PubMed1990

The three operators of the lac operon cooperate in repression.

We tested the effect of systematic destruction of all three lac operators of the chromosomal lac operon of Escherichia coli on repression by Lac repressor. Absence of just one 'pseudo-operator' O2 or O3 decreases repression by wild-type tetrameric Lac repressor approximately 2- to 3-fold; absence of both 'pseudo-operators' decreases repression greater than 50-fold. O1 alone represses under these conditions only approximately 20-fold. Dimeric active Lac repressor (iadi) represses the wild-type lac operon to about the same low extent. This indicates that cooperative interaction between lac operators is due to DNA loop formation mediated by tetrameric Lac repressor. Under conditions where loop formation is impossible, occupation of O3 but not of O2 may lead to weak repression. This suggests that under these conditions CAP activation may be inhibited and that stopping transcription at O2 does not significantly contribute to repression.

Base Sequence↗
PubMed1994

Differential repression of transcription factor binding by histone H1 is regulated by the core histone amino termini.

In order to investigate the interrelated roles of nucleosome cores and histone H1 in transcription repression, we have employed a purified system to analyze the function of H1 in the repression of transcription factor binding to nucleosomes. H1 binding to nucleosome cores resulted in the repression of USF binding to nucleosomes. By contrast, H1 only slightly inhibited the binding of GAL4-AH, indicating that H1 differentially represses the binding of factors with different DNA-binding domains. H1-mediated repression of factor binding was dependent on the core histone amino-terminal tails. Removal of these domains alleviated H1-mediated repression and increased acetylation of these domains partly alleviated repression by H1. H1 binding assays suggest a less stable interaction of histone H1 with the core particle in the absence of the amino termini.

Acetylation↗