Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ultraviolet light (UV) survival curve of Escherichia coli WP10 recA trp is almost biphasic, with a greatly reduced shoulder but demonstrating a transition to a decreased slope with increasing fluences, indicating the presence in the culture of a low frequency of resistant cells. Treatment of the culture with chloramphenicol before UV exposure brought almost all of the cells to a high degree of UV resistance, by bringing them to the end of their DNA replication cycle. The survival curves of the repair-proficient E. coli WP2 trp showed a similar pattern with chloramphenicol treatment or tryptophan starvation before UV exposure, but only if protein synthesis were blocked by chloramphenicol for 60 min after UV exposure. The results suggest that when recA/lexA-regulon induction is prevented, either by the recA mutation or by inhibition of protein synthesis after UV exposure, death occurs unless the cells are in the resistant state characteristic of bacteria at the end of their DNA replication cycle. With repair-proficient bacteria treated before UV exposure with chloramphenicol, when protein synthesis is not blocked after UV exposure, a marked expansion of the shoulder occurs because of the function of another resistance-conferring mechanism. This mechanism also depends on the recA+ gene since expansion of the shoulder does not occur in recA bacteria when protein synthesis is inhibited before UV exposure.
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PMID:Evidence that ultraviolet light-induced DNA replication death of recA bacteria is prevented by protein synthesis in repair-proficient bacteria. 264 26

Two regulatory proteins, PHO2 and the general control regulator GCN4, bind in vitro to the promoter of the tryptophan biosynthetic TRP4 gene; the TRP4 gene product catalyses the phosphoribosylation of anthranilate. PHO2 binds specifically to the TRP4 promoter, but does not bind to any other TRP promoter. PHO2 and GCN4 proteins bind in a mutually exclusive manner to the same sequence, UAS1, one of two GCN4 binding sites in the TRP4 promoter. UAS1 is the major site for GCN4-dependent TRP4 activation. The second GCN4 binding site, UAS2, interacts with GCN4 alone. PHO2 binding interferes with the general control response of TRP4 under low phosphate conditions and simultaneous amino acid starvation and thus the PHO2 regulatory protein connects phosphate metabolism and amino acid biosynthesis in yeast. The GCN4 protein mediates the response of the transcriptional apparatus to the environmental signal 'amino acid limitation', while PHO2 seems to be the phosphate sensor that adjusts the response to the availability of phosphate precursors.
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PMID:Interpathway regulation of the TRP4 gene of yeast. 265 61

Male SPF Wistar rats adapted to a 12:12 h light: dark regimen were irradiated at 3-hour intervals in the course of 24 h with a dose of 14.35 Gy X-rays; 24 h after irradiation or sham irradiation and starvation for the same length of time, and also in fed intact rats, tyrosine aminotransferase and tryptophan-2-3-dioxygenase activity in the liver and the serum corticosterone level were determined. Although lethal irradiation modified the given enzyme activities, it did not abolish their circadian rhythm, evidently in association with the low sensitivity in association with the low sensitivity of the liver to ionizing radiation. In irradiated animals (compared with sham-irradiated animals), the serum corticosterone concentration fell during the light part of the day and at the beginning of the dark part.
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PMID:Correlation of circadian changes in tyrosine aminotransferase and tryptophan-2-3-dioxygenase in rat liver to irradiation at different times of the day. 288 71

The effect of human recombinant interferon-gamma (IFN-gamma) on Toxoplasma gondii in cultured human fibroblasts is predominantly parasitostatic. This effect is dependent upon the induction in the host cell of a potent indoleamine 2,3-dioxygenase that converts tryptophan to N-formylkynurenine. This product is, in turn, degraded to kynurenine by a formamidase. Within 24 h of treatment with IFN-gamma most of the tryptophan originally present in the medium is converted to these products together with some minor metabolites. When added to the medium of infected cultures at concentrations equimolar to the tryptophan content, neither N-formylkynurenine nor kynurenine suppresses the growth of T. gondii, although at higher concentrations they are effective. The medium of uninfected cultures treated with IFN-gamma for 24 h has no effect on the growth of T. gondii, when transferred to fresh cultures provided that the residual IFN-gamma is first removed by ultrafiltration or neutralized with a specific monoclonal antibody. Thus minor metabolites produced from tryptophan in response to IFN-gamma and excreted into the medium are not parasitostatic. When cultures treated with IFN-gamma for 24 h are incubated with medium that contains [3H]tryptophan, the radioactive amino acid is converted to N-formylkynurenine and kynurenine as rapidly as it enters the cell. This degradation not only results in a very low intracellular concentration of tryptophan but also produces intracellular concentrations of tryptophan metabolites that are significantly higher than the tryptophan concentration in control cells. However, it is unlikely that either metabolite reaches intracellular concentrations that are sufficient to suppress the growth of the parasite. The parasitostatic effect of IFN-gamma is most likely to result from the starvation of T. gondii for tryptophan.
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PMID:Interferon-gamma suppresses the growth of Toxoplasma gondii in human fibroblasts through starvation for tryptophan. 309 59

The addition of DL-7-azatryptophan (AZAT), a tryptophan analog, to continuous cultures of Anabaena sp. strain CA grown with 10 mM nitrate as the nitrogen source resulted in the differentiation of heterocysts. Analysis of the intracellular amino acid pools of Anabaena sp. strain CA after the addition of AZAT showed a marked decline in the intracellular glutamate pool and a slight increase in the levels of glutamine. The in vitro activity of glutamate synthase, the second enzyme involved in primary ammonia assimilation in Anabaena spp., was partially inhibited by the presence of AZAT at concentrations which are effective in triggering heterocyst formation (15% inhibition at 10 microM AZAT and up to 85% inhibition at 1.0 mM AZAT). Azaserine, a glutamine analog and potent glutamate synthase inhibitor, had no effect on the triggering of heterocyst development from undifferentiated batch and continuous cultures of Anabaena sp. strain CA. However, the presence of 1.0 microM azaserine significantly decreased the intracellular glutamate pool and increased the glutamine pool. The addition of AZAT also caused a decrease in the C-phycocyanin content of Anabaena sp. strain CA as a result of its proteolytic degradation. AZAT also had an inhibitory effect on the nitrogenase activity of Anabaena sp. strain CA. All these results suggest that AZAT causes a general nitrogen starvation of Anabaena sp. strain CA filaments, triggering heterocyst synthesis.
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PMID:Nitrogen starvation mediated by DL-7-azatryptophan in the cyanobacterium Anabaena sp. strain CA. 310 56

The threonine deaminase gene (ILV1) of Saccharomyces cerevisiae has been designated "multifunctional" since Bollon (1974) indicated its involvement both in the catalysis of the first step in isoleucine biosynthesis and in the regulation of the isoleucine-valine pathway. Its role in regulation is characterized by a decrease in the activity of the five isoleucine-valine enzymes when cells are grown in the presence of the three branched-chain amino acids, isoleucine, valine and leucine (multivalent repression). We have demonstrated that the regulation of AHA reductoisomerase (encoded by ILV5) and branched-chain amino acid transaminase is unaffected by the deletion of ILV1, subsequently revealing that the two enzymes can be regulated in the absence of threonine deaminase. Both threonine deaminase activity and ILV1 mRNA levels increase in mutants (gcd2 and gcd3) having constitutively depressed levels of enzymes under the general control of amino acid biosynthesis, as well as in response to starvation for tryptophan and branched-chain amino acid imbalance. Thus, the ILV1 gene is under general amino acid control, as is the case for both the ILV5 and the transaminase gene. Multivalent repression of reductoisomerase and transaminase can be observed in mutants defective in general control (gcn and gcd), whereas this is not the case for threonine deaminase. Our analysis suggests that repression effected by general control is not complete in minimal medium. Amino acid dependent regulation of threonine deaminase is only through general control, while the branched-chain amino acid repression of AHA reducto isomerase and the transaminase is caused both by general control and an amino acid-specific regulation.
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PMID:Regulation of isoleucine-valine biosynthesis in Saccharomyces cerevisiae. 328 62

A decline in colony-forming ability is observed in actively growing cultures of a tryptophan arginine auxotroph of Bacillus subtilis after removal of tryptophan (tryptophanless death). This phenomenon can be prevented by simultaneous starvation of the other required amino acid or by chloramphenicol administered in bacteriostatic concentration but not by actinomycin. Addition of tryptophan analogues not only prevents the death but also allows recovery of the cells that have lost the ability to form colonies on solid media. The term tryptophanless death is therefore inappropriate. Chloramphenicol but not actinomycin inhibits the recovery brought about by tryptophan analogues.
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PMID:Tryptophanless death in Bacillus subtilis. 418 6

Polysomes were extracted from Bacillus subtilis cells starved for a required amino acid. The monosome peak appeared soon after starvation; no difference in the rate of degradation was detected when the cells were starved for arginine or tryptophan in a double auxotroph. RNA production during starvation was not inhibited by actinomycin, but the molecular weight of the product made in the presence of the antibiotic was much lower. Indications that stable messenger ribonucleic acid is present for up to 90 min after amino acid starvation are also presented.
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PMID:Polyribosomes from Bacillus subtilis during amino acid starvation in the presence and in the absence of actinomycin. 419 20

A tryptophan-requiring auxotroph of Agmenellum quadruplicatum strain BG1, a species of blue-green bacteria, was isolated by means of a nitrosoguanidine-penicillin procedure. Its growth characteristics were determined, and the enzymological block was identified in the A activity of tryptophan synthetase. Starvation of the auxotroph for tryptophan resulted in the derepression of the synthesis of all five enzymes. The first four enzymes derepressed 2- to 3-fold, and tryptophan synthetase B derepressed 20-fold. In the parental prototroph, BG1, anthranilate synthetase was active in crude extracts with ammonia as the amino donor reactant, but not with glutamine.
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PMID:Documentation of auxotrophic mutation in blue-green bacteria: characterization of a tryptophan auxotroph in Agmenellum quadruplicatum. 420 2

Inhibitors of protein synthesis do not consistently prevent formation of the lac operon repressor, according to several published reports, although direct evidence indicates that the repressor is a protein. Inhibition of ribonucleic acid (RNA) synthesis has never been shown to block lactose repression. These results have raised the possibility that repressor is synthesized in some unusual fashion. We have studied the effect of various inhibitors upon the establishment of repression in zygotes, utilizing conditions which minimize catabolite repression. Inhibition of protein synthesis by either chloramphenicol treatment or tryptophan deprivation blocked repressor formation in our experiments. Sodium borate and 6-azauracil are compounds reported to be specific inhibitors of RNA synthesis, and their behavior in control experiments is consistent with this specificity. Both delayed the establishment of repression. Thymine deprivation, either by starvation of a thymine auxotroph or by treatment with 5-fluorodeoxyuridine, did not delay the onset of repression. We conclude that repressor formation requires RNA synthesis and probably utilizes the usual protein-forming mechanisms.
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PMID:Requirements for macromolecular synthesis in the establishment of beta-galactosidase repression in zygotes. 423 Dec 83


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