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PubMed2003

The constitutional t(17;22): another translocation mediated by palindromic AT-rich repeats.

We have demonstrated that the breakpoints of the constitutional t(11;22) are located at palindromic AT-rich repeats (PATRRs) on 11q23 and 22q11. As a mechanism for this recurrent translocation, we proposed that the PATRR forms a cruciform structure that induces the genomic instability leading to the rearrangement. A patient with neurofibromatosis type 1 (NF1) had previously been found to have a constitutional t(17;22) disrupting the NF1 gene on 17q11. We have localized the breakpoint on 22q11 within the 22q11-specific low-copy repeat where the breakpoints of the constitutional t(11;22)s reside, implying a similar palindrome-mediated mechanism for generation of the t(17;22). The NF1 gene contains a 195-bp PATRR within intron 31. We have isolated the junction fragments from both the der(17) and the der(22). The breakpoint on 17q11 is close to the center of the PATRR. A published breakpoint of an additional NF1-afflicted patient with a constitutional t(17;22) is also located close to the center of the same PATRR. Our data lend additional support to the hypothesis that PATRR-mediated genomic instability can lead to a variety of translocations.

Base Sequence↗
PubMed1988

A constitutive member of the rat cytochrome P450IIB subfamily: full-length coding sequence of the P450IIB3 cDNA.

The prototypic members of the rat liver cytochrome P450IIB subfamily, P450b and P450e, have long been the subjects of intense interest, in part because they are highly inducible by phenobarbital (PB). We have previously cloned and sequenced an 858-bp cDNA fragment (the PB24 insert) that encodes the carboxy-terminal portion of a P450b/P450e-like protein, henceforth referred to as P450IIB3. A Bam HI-Eco RI fragment of the PB24 insert hybridizes with a 1.9-kb mRNA present constitutively in rat liver and not inducible by PB (Affolter et al., 1986). We have now obtained, from a lambda gt11 rat liver cDNA library, cDNA inserts corresponding to the complete coding sequence of the IIB3 mRNA. The 491-amino acid IIB3 protein sequence, deduced from the cDNA sequence, is 77% identical to that of P450b. Northern blot analysis, with a IIB3-specific oligonucleotide probe, confirmed the constitutive presence of the polyadenylated 1.9-kb IIB3 mRNA in male rat liver. The IIB3 mRNA was undetectable in the lung, kidney, and prostate. It was constitutively present, and not inducible by PB, in female rat liver. Our results demonstrate unequivocally the existence of a constitutive member of the rat P450IIB subfamily. The remarkable inducibility of the P450b/P450e genes is in striking contrast to the absence of a PB effect on IIB3 gene expression. The molecular basis for this difference remains to be revealed.

Amino Acid Sequence↗
PubMed1985

The generation of stable human T-cell hybridomas which constitutively produce interleukin-2 and chemotactic factor.

We report the successful generation of human T-cell hybridomas that constitutively secrete lymphokines. An acute lymphoblastic leukemia T-cell line, CCRF-H-SB2, free of reverse transcriptase and mycoplasma, was sensitized to hypoxanthine, aminopterin, and thymidine (HAT) by selecting out a mutant deficient in hypoxanthine guanine phosphoribosyl transferase (HGPRT) in 8-azaguanine. Peripheral blood T lymphocytes from normal donors were incubated in vitro with 10 micrograms/ml of concanavalin A for 48 h and subsequently fused with the CCRF-H-SB2 HAT-sensitive cell line. Following 5 weeks in culture, 38 of 440 wells (8.6%) demonstrated hybridoma growth. Supernatants of these cultures were screened for interleukin-2 (IL-2), chemotactic factor, interferon, migration inhibition factor, and macrophage-activating factor activities. Twelve (of 38) hybrids exhibited IL-2 activity, and eight of these were successfully cloned. The highest secreting clone was demonstrated to have mRNA to IL-2 while the parent CCRF-H-SB2 had no detectable mRNA to IL-2. Three hybrid cultures produced chemotactic factor; one was successfully cloned and grown in serum-free medium, where it continued to constitutively produce chemotactic factor as well as IL-2 activity. The chemotactic factor was determined to have the same molecular weight (12,500 daltons) as leukocyte-derived chemotactic factor. Constitutive IL-2 production remained stable for over 12 months. None of the hybridomas tested produced detectable levels of gamma interferon, migration inhibition factor, or macrophage activation factor. Because these T-cell hybridomas produce lymphokines constitutively and this phenotype is stable, they can be an important source of highly purified human lymphokines for clinical and laboratory investigations.

Antigens, Surface↗
PubMed2003

Reduced constitutive 8-oxoguanine-DNA glycosylase expression and impaired induction following oxidative DNA damage in the tuberin deficient Eker rat.

The Tsc-2 tumor suppressor gene encodes the protein tuberin, a multi-functional protein with sequence homology to the GTPase activating protein (GAP) for Rap1. Mutations in the Tsc-2 gene are associated with the development of renal tumors. The Eker rat (Tsc-2(EK/+)) bears a mutation in one allele of the Tsc-2 gene, which predisposes these animals to renal cancer. Treatment of wild-type (Tsc-2(+/+)) and mutant (Tsc-2(EK/+)) Eker rats with 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ; 7.5 micro mol/kg. i.v.), a potent redox active and nephrotoxic metabolite of hydroquinone increases the incidence of renal tumors only in animals carrying the mutant Tsc-2(EK/+) allele. We now show that the constitutive expression of 8-oxoguanine-DNA glycosylase (OGG1) in Tsc-2(EK/+) rats is three-fold lower than in wild-type Tsc-2(+/+) rats. Moreover, treatment of wild-type and mutant Eker rats with TGHQ greatly increases 8-oxo-deoxyguanosine (8-oxo-dG) levels within the outer stripe of the outer medulla. Tsc-2(EK/+) rats, with lower constitutive renal OGG1 expression, experience substantially higher levels of 8-oxo-dG than do wild type Tsc-2(+/+) rats. Interestingly, whereas OGG1 expression was rapidly (4 h) induced in Tsc-2(+/+) rats following exposure to TGHQ, it was significantly reduced in Tsc-2(EK/+) rats. The combination of the higher constitutive expression of OGG1 in Tsc-2(+/+) rats, and its rapid induction in response to TGHQ treatment, coupled to the initial decrease in OGG1 expression in Tsc-2(EK/+) rats, results in Tsc-2(EK/+) OGG1 protein levels just 5% of those seen in Tsc-2(+/+) rats 8 h after treatment. Coincidentally, 8-oxo-dG levels in Tsc-2(+/+) rats 8 h after treatment with TGHQ are just 5% of those that occur in Tsc-2(EK/+) rats. The results indicate that the Tsc-2 gene influences constitutive OGG1 expression and the ability of OGG1 to respond to an oxidative stress, consistent with the proposal that Tsc-2 is an acute-phase response gene. In keeping with this view, acute TGHQ-induced cytotoxicity was greater in Tsc-2(EK/+) rats than in Tsc-2(+/+) rats. The mechanism(s) coupling tuberin expression to the regulation of OGG1 are not known and are under investigation.

Animals↗
PubMed2006

Constitutive expression of functionally active cyclin-dependent kinases and their binding partners suggests noncanonical functions of cell cycle regulators in differentiated neurons.

Neurodegeneration in Alzheimer's disease and various experimental lesion paradigms are associated with an unscheduled upregulation of cell cycle-related proteins, indicating a link between cell cycle reactivation and neuronal death. Recent evidence, however, suggests that at least some of the canonical cell cycle regulators are constitutively expressed in differentiated neurons of the adult brain. Systematic investigations on the constitutive expression of cell cycle regulators in differentiated neurons in vivo, providing the basis for further insights into their potential role under pathological conditions, however, have not been carried out. Here, we demonstrate a constitutive neuronal expression of Cdks 1, 2, and 4; their activators cyclins D, A, B, and E; and their inhibitors p15(Ink4b), p16(Ink4a), p18(Ink4c), p19(Ink4d), p21(Waf1/Cip1), p27(Kip1), and p57(Kip2) within the neocortex of adult mice by western blot and immunocytochemistry. Expression was verified by single-cell reverse transcriptase-polymerase chain reaction applied to individual microscopically identified neurons captured with laser dissection. Immunoprecipitation and in vitro kinase assays revealed that Cdks 1, 2, and 4 are properly complexed to cyclins and exhibit kinase activity. This physiological expression of positive cell cycle regulators in adult neurons is clearly not related to neuronal proliferation. Taken together, our findings demonstrate a constitutive expression of functionally active cyclin-dependent kinases and their regulators in differentiated neurons suggesting a noncanonical role of cell cycle regulators potentially linked to neuronal plasticity and/or stability.

Animals↗
PubMed2001

Constitutively active mutants of 5-HT4 receptors are they in unique active states?

Somatic mutations leading to constitutively active G-protein coupled receptors (GPCRs) are responsible for certain human diseases. A consistent structural description of the molecular change underlying the conversion of GPCRs from an inactive R state to an active R* state is lacking. Here, we show that a series of constitutively active 5-HT4 receptors (mutated or truncated in the C-terminal and the third intracellular loop) were characterized by an increase in their denaturation rate at 55 degrees C. The thermal denaturation kinetics were monophasic, suggesting that we were measuring mainly the denaturation rate of R*. Analysis of these kinetics revealed that constitutively active C-terminal domain mutants, were due to a change in the J constant governing the R/R* equilibrium. However, the constitutive activity of the receptor mutated within the third intracellular loop was the result of both a change in the allosteric J constant and a change in the R* conformation.

Animals↗
PubMed1997

A mutation mimicking ligand-induced conformational change yields a constitutive RXR that senses allosteric effects in heterodimers.

Mutations of a single residue in the retinoid X receptor alpha (RXRalpha) ligand-binding pocket (LBP) generate constitutive, ligand-binding-competent mutants with structural and functional characteristics similar to those of agonist-bound wild-type RXR. Modelling of the mouse RXRalphaF318A LBP suggests that, like agonist binding, the mutation disrupts a cluster of van der Waals interactions that maintains helix H11 in the apo-receptor location, thereby shifting the thermodynamic equilibrium to the holo form. Heterodimerization with some apo-receptors (retinoic acid, thyroid hormone and vitamin D3 receptors) results in 'silencing' of RXRalphaF318A constitutive activity, which, on the other hand, efficiently contributes to synergistic transactivation within NGFI-B-RXR heterodimers. RAR mutants disabled for corepressor binding and/or lacking a functional AF-2 activation domain, do not relieve RXR 'silencing'. Not only RAR agonists, but also the RAR antagonist BMS614 induce conformational changes allowing RXR to exert constitutive (RXRalphaF318A) or agonist-induced (wild-type RXR) activity in heterodimers. Interestingly, the RXRalphaF318A constitutive activity generated within heterodimers in the presence of BMS614 requires the integrity of both RXR and RAR AF-2 domains. These observations suggest that, within RXR-RAR heterodimers, RAR can adopt a structure distinct from that of the active holo-RAR, thus allowing RXR to become transcriptionally responsive to agonists.

Allosteric Regulation↗
PubMed1999

Constitutive silencing of IFN-beta promoter is mediated by NRF (NF-kappaB-repressing factor), a nuclear inhibitor of NF-kappaB.

Transcriptional regulation of the interferon-beta (IFN-beta) gene is characterized by strict constitutive repression and virus-specific activation. Previous studies have shown that the IFN-beta promoter is constitutively repressed by a negative regulatory element (NRE). Isolated NRE acts as a constitutive and position-independent silencer on the NF-kappaB-binding sites. Here, we describe the identification and functional characterization of the NRE-binding protein, called NRF (NF-kappaB-repressing factor), which abolishes the transcriptional activity of the bordering NF-kappaB- binding sites by a distance-independent mechanism. Deletion studies show that a minimal repression domain of NRF is sufficient to exert its inhibitory effect. In vitro, NF-kappaB proteins bind to purified NRF by a direct protein-protein interaction. We demonstrate that NRF is a ubiquitous and constitutive nuclear protein. In fibroblasts, the expression of the NRF antisense RNA releases the endogenous IFN-beta gene transcription. Our data strongly suggest that the NRF-mediated inhibition of NF-kappaB is a critical component of the IFN-beta gene silencing prior to viral infection.

Amino Acid Sequence↗
PubMed2000

How Stat1 mediates constitutive gene expression: a complex of unphosphorylated Stat1 and IRF1 supports transcription of the LMP2 gene.

Analysis of mRNA levels in cells that express or lack signal transducers and activators of transcription 1 (Stat1) reveals that Stat1 mediates the constitutive transcription of many genes. Expression of the low molecular mass polypeptide 2 (LMP2), which requires Stat1, has been studied in detail. The overlapping interferon consensus sequence 2/gamma-interferon-activated sequence (ICS-2/GAS) elements in the LMP2 promoter bind to interferon regulatory factor 1 (IRF1) and Stat1 and are occupied constitutively in vivo. The point mutant of Stat1, Y701F, which does not form dimers involving SH2-phosphotyrosine interactions, binds to the GAS element and supports LMP2 expression. Unphosphorylated Stat1 binds to IRF1 directly and we conclude that this complex uses the ICS-2/GAS element to mediate constitutive LMP2 transcription in vivo. The promoter of the IRF1 gene, which also contains a GAS site but not an adjacent ICS-2 site, is not activated by Stat1 Y701F. The promoters of other genes whose constitutive expression requires Stat1 may also utilize complexes of unphosphorylated Stat1 with IRF1 or other transcription factors.

Base Sequence↗
PubMed1987

The constitutive, glucose-repression-insensitive mutation of the yeast MAL4 locus is an alteration of the MAL43 gene.

Mutations resulting in constitutive production of maltase have been identified at each of the five MAL loci of Saccharomyces yeasts. Here we examine a dominant constitutive, glucose-repression-insensitive allele of the MAL4 locus (MAL4-C). Our results demonstrate that MAL4-C is an alteration in the MAL43 gene, which encodes the positive regulator of the MAL structural genes, and that its product is trans-acting. The MAL43 gene from the MAL4-C strain was cloned and integrated into a series of nonfermenting strains lacking a functional regulatory gene but carrying copies of the maltose permease and maltase structural genes. Expression of the maltase structural gene was both constitutive and insensitive to glucose repression in these transformants. The MAL4-C allele also results in constitutive expression of the unlinked MAL12 gene (encoding maltase) in this strain. In addition, the cloned MAL43 gene was shown to be dominant to the wild-type MAL63 gene. We also show that most of the glucose repression insensitivity of strains carrying the MAL4-C allele results from alteration of MAL43.

Chromosome Deletion↗
PubMed2006

Molecular analysis of constitutively expressed erm(C) genes selected in vitro in the presence of the non-inducers pirlimycin, spiramycin and tylosin.

OBJECTIVES: As known from other lincosamides and 16-membered macrolides, the antimicrobial agents pirlimycin, spiramycin and tylosin, which are frequently used for the therapy of bovine mastitis, cannot induce the expression of the resistance gene erm(C). The aim of this study was to confirm the ability of these three non-inducers to select for constitutively expressed erm(C) mutants in Staphylococcus aureus. METHODS: A S. aureus strain carrying an inducibly expressed erm(C) gene was incubated on agar plates containing inhibitory concentrations of each of the three antimicrobial agents. The erm(C) regulatory region of mutants obtained after overnight incubation was amplified by PCR; selected amplicons were sequenced and compared with the wild-type sequence. RESULTS: Mutants developed in the presence of each of the three antimicrobial agents. Constitutive expression of erm(C) was due to variations in the erm(C) regulatory region. A total of 10 different types of deletions ranging in size between 16 and 121 bp as well as 20 different types of duplications ranging between 24 and 602 bp were detected. The frequencies by which sequence alterations occurred as well as the types of alterations detected varied with regard to the antimicrobial agents used for selection. CONCLUSIONS: All sequence alterations observed explained constitutive erm(C) gene expression by functional inactivation of translational attenuation. In order to prevent the development of constitutively resistant isolates under therapy, the results of this study support the recommendation not to use lincosamides or 16-membered macrolides for the control of staphylococcal infections caused by strains harbouring inducibly expressed erm(C) genes.

Animals↗
PubMed1999

Dietary protein or arginine deficiency impairs constitutive and inducible nitric oxide synthesis by young rats.

Effects of dietary protein or arginine deficiency on constitutive and lipopolysaccharide (LPS)-induced nitric oxide (NO) synthesis were determined in young rats by quantifying urinary nitrate excretion. In Experiment 1, 30-d-old rats (n = 16) were divided randomly into two groups (n = 8/group) and pair-fed on the basis of body weight semipurified isocaloric diets containing 20 or 5% casein. In Experiment 2, 30-d-old rats (n = 24) were divided randomly into three groups (n = 8) and pair-fed on the basis of body weight purified isonitrogenous and isocaloric diets (composed of amino acids) containing 0.0, 0.3 or 1.0% L-arginine. In both experiments, daily collection of urine was initiated 10 d after the start of pair-feeding. On d 17 after the pair-feeding was initiated, LPS (1 mg/kg body wt) was injected intraperitoneally into rats, and urine was collected daily for an additional 7 d. In Experiments 3 and 4, activities of constitutive and inducible NO synthases were measured in macrophages and various tissues from protein- or arginine-deficient rats (n = 6). Body weight was lower in rats fed the 5% casein diet or the 0.0 and 0.3% arginine diets than in those fed 20% casein or 1% arginine, respectively. Dietary protein or arginine deficiency decreased serum concentrations of arginine and urinary nitrate excretion before and after LPS treatment, indicating impaired constitutive and inducible NO synthesis. Protein malnutrition reduced constitutive and inducible NO synthase activities in brain, heart, jejunum, lung, skeletal muscle and spleen, and inducible NO synthase activity in macrophages. Because NO is a mediator of the immune response and is the endothelium-dependent relaxing factor, impaired NO synthesis may help explain immunodeficiency and cardiovascular dysfunction in protein- or arginine-deficient subjects.

Amino Acids↗
PubMed2002

Transcription initiation in vivo without classical transactivators: DNA kinks flanking the core promoter of the housekeeping yeast adenylate kinase gene, AKY2, position nucleosomes and constitutively activate transcription.

The housekeeping gene of the major adenylate kinase in Saccharomyces cerevisiae (AKY2, ADK1) is constitutively transcribed at a moderate level. The promoter has been dissected in order to define elements that effect constitutive transcription. Initiation of mRNA synthesis at the AKY2 promoter is shown to be mediated by a non-canonic core promoter, (TA)(6). Nucleotide sequences 5' of this element only marginally affect transcription suggesting that promoter activation can dispense with transactivators and essentially involves basal transcription. We show that the core promoter of AKY2 is constitutively kept free of nucleosomes. Analyses of permutated AKY2 promoter DNA revealed the presence of bent DNA. DNA structure analysis by computer and by mutation identified two kinks flanking an interstitial stretch of 65 bp of moderately bent core promoter DNA. Kinked DNA is likely incompatible with packaging into nucleosomes and responsible for positioning nucleosomes at the flanks allowing unimpeded access of the basal transcription machinery to the core promoter. The data show that in yeast, constitutive gene expression can dispense with classical transcriptional activator proteins, if two prerequisites are met: (i) the core promoter is kept free of nucleosomes; this can be due to structural properties of the DNA as an alternative to chromatin remodeling factors; and (ii) the core promoter is pre-bent to allow a high rate of basal transcription initiation.

5' Flanking Region↗
PubMed2001

Activation of an EDS1-mediated R-gene pathway in the snc1 mutant leads to constitutive, NPR1-independent pathogen resistance.

The Arabidopsis NPR1 protein is an essential regulatory component of systemic acquired resistance (SAR). Mutations in the NPR1 gene completely block the induction of SAR by signals such as salicylic acid (SA). An Arabidopsis mutant, snc1 (suppressor of npr1-1, constitutive 1), was isolated in a screen for suppressors of npr1-1. In the npr1-1 background, the snc1 mutation resulted in constitutive resistance to Pseudomonas syringae maculicola ES4326 and Peronospora parasitica Noco2. High levels of SA were detected in the mutant and shown to be required for manifestation of the snc1 phenotype. The snc1 mutation was mapped to the RPP5 resistance (R) gene cluster and the eds1 mutation that blocks RPP5-mediated resistance suppressed snc1. These data suggest that a RPP5-related resistance pathway is activated constitutively in snc1. This pathway does not employ NPR1 but requires the signal molecule SA and the function of EDS1. Moreover, in snc1, constitutive resistance is conferred in the absence of cell death, which is often associated with R-gene mediated resistance.

Arabidopsis↗
PubMed2003

Interindividual variations in constitutive interleukin-10 messenger RNA and protein levels and their association with genetic polymorphisms.

BACKGROUND: Genetic variations in the interleukin (IL)-10 gene promoter have been associated with levels of induced production of IL-10, disease susceptibility, and allograft rejection. Small amounts of this cytokine are constitutively produced and are important in maintaining the physiologic function of the cytokine network. In this study, we evaluated the distribution of IL-10 basal levels and its genetic regulation in a healthy Spanish population. METHODS: Polymorphisms at the -1,082, -819, and -512 positions of the IL-10 promoter were analyzed by polymerase chain reaction amplification and hybridization with fluorescent-labeled allele-specific probes in 183 Spanish people. Levels of IL-10 messenger (m)RNA were tested by real-time reverse transcription-polymerase chain reaction in 123 healthy donors. Serum concentrations of IL-10 were measured by a highly sensitive ELISA, whereas protein amounts in lipopolysaccharide culture supernatants were quantified by an in-house ELISA. RESULTS: The frequency of IL-10 promoter alleles and haplotypes in our population showed remarkable differences from other Caucasian populations. Large interindividual variations were found in mRNA and protein constitutive levels of IL-10, which allowed its classification in low and intermediate/high producers. We found statistical differences in mRNA concentration between the polymorphic variant GCC/GCC and the low producer genotypes. The G allele at position -1082 was the most important genetic factor in the regulation of constitutive IL-10 mRNA levels. Similarly, we also found an association of this polymorphic position with serum concentration greater than 2 pg/mL. CONCLUSIONS: Constitutive levels of IL-10 (mRNA and serum protein) displayed remarkable interindividual variations, which are genetically controlled by polymorphic variants at the cytokine gene promoter.

Alleles↗
PubMed2006

Instabilities and constitutive modelling.

The plastics industry today sees huge wastage through product defects caused by unstable flows during the manufacturing process. In addition, many production lines are throughput-limited by a flow speed threshold above which the process becomes unstable. Therefore, it is critically important to understand the mechanisms behind these instabilities. In order to investigate the flow of a molten plastic, the first step is a model of the liquid itself, a relation between its current stress and its flow history called a constitutive relation. These are derived in many ways and tested on several benchmark flows, but rarely is the stability of the model used as a criterion for selection. The relationship between the constitutive model and the stability properties of even simple flows is not yet well understood. We show that in one case a small change to the model, which does not affect the steady flow behaviour, entirely removes a known instability. In another, a change that makes a qualitative difference to the steady flow makes only tiny changes to the stability.The long-term vision of this research is to exactly quantify what are the important properties of a constitutive relation as far as stability is concerned. If we could understand that, not only could very simple stability experiments be used to choose the best constitutive models for a particular material, but our ability to predict and avoid wasteful industrial instabilities would also be vastly improved.

Journal Article↗
PubMed1999

Human parainfluenza virus type 1 phosphoprotein is constitutively phosphorylated at Ser-120 and Ser-184.

RNA-dependent RNA polymerases of single-stranded, negative-sense RNA viruses comprise a phosphoprotein (P) and a large protein. The constitutive phosphorylation of the P protein in these viruses is highly conserved, yet the functional significance of phosphorylation is enigmatic. To approach this problem, phosphorylation sites were determined in two closely related paramyxovirus P proteins. Sendai virus (SV) is a prototypic paramyxovirus. Previously, using a phosphopeptide mapping technique, the primary constitutive phosphorylation site of SV P protein was mapped to Ser-249. Phosphorylation at Ser-249 is dependent on the presence of Pro-250. Human parainfluenza virus type 1 (HPIV-1) P protein has 66% similarity to SV P protein and its predicted secondary structure is highly similar to that of SV P protein. However, there is no obvious conserved phosphorylation site in HPIV-1 P protein. Using the phosphopeptide mapping strategy, the constitutive phosphorylation sites of HPIV-1 P protein were mapped. The HPIV-1 P protein is primarily phosphorylated at Ser-120. Phosphorylation at Ser-120 is dependent on the presence of Pro-121. It also has a minor phosphorylation site at Ser-184. The sequence at Ser-184 does not match any consensus phosphorylation target site for the known kinases. Significantly, the P proteins from both viruses are constitutively and primarily phosphorylated at one serine and the phosphorylation of that serine is dependent on the presence of a proline on its carboxyl side.

Amino Acid Sequence↗
PubMed1978

Mutants of Acinetobacter calcoaceticus NCIB 8250 constitutive for the mandelate enzymes.

Methods for isolating mutants of Acinetobacter calcoaceticus NCIB 8250 constitutive for the mandelate enzymes were compared. Non-inducing substrates were not available. Continuous culture gave no stable constitutive mutants. Alternate culture in inducing (L-mandelate) and non-inducing (L-glutamate) media led to the isolation of mutants mesoconstitutive for L-mandelate dehydrogenase and phenylgloxylate carboxy-lyase, and hyperinducible for benzaldehyde dehydrogenase I. Screening of possible anti-inducers showed that 2-phenyl-propionate was very effective; it was a competitive inhibitor of gratuitous induction by thiophenoxyacetate, and was used for the isolation of constitutive mutants. Some of the mutants were magnoconstitutive for L-mandelate dehydrogenase, phenylglyoxylate carboxylyase and benzaldehyde dehydrogenase I and could not be further induced; others had lower specific activities which could be increased by induction with phenylglyoxylate or thiophenoxyacetate. Similar constitutive mutants were derived from a mutant which lacked L-mandelate dehydrogenase.

Acinetobacter↗