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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In Salmonella typhimurium, as in Escherichia coli, mutations in avtA, the gene encoding the alanine-valine transaminase (transaminase C), are silent unless they are combined with mutations involved in isoleucine-valine biosynthesis. avtA is repressed by leucine or alanine but not by valine. Transaminase C is found at reduced levels upon starvation for any one of several amino acids. We hypothesize that this is due to repression of avtA by the elevated alanine and leucine pools found in amino acid-starved cells.
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PMID:Role of alanine-valine transaminase in Salmonella typhimurium and analysis of an avtA::Tn5 mutant. 630 35

The effect of cell cycle on Rb+ (K+) fluxes was studied in NIH 3T3 mouse fibroblasts. Serum starvation or isoleucine deprivation resulted in cell arrest at an early G1/G0 phase, accompanied by a marked decrease in both ouabain-sensitive and ouabain-resistant Rb+ influx. On the other hand, cells arrested at late G1/G0 phase by hydroxyurea treatment have high ouabain-sensitive and ouabain-resistant Rb+ influx. Butyric acid treatment resulted in cell arrest at an early G1/G0 phase, but in contrast to serum or isoleucine starvation did not decrease Rb+ influxes. It is thus shown that quiescent cells may have Rb+ influx rates as high as that of logarithmically growing cells. The results are consistent with the hypothesis that an increased ion permeability of the cell is initiated at a critical stage in G1/G0 phase, and that butyric acid may arrest the cell beyond that stage.
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PMID:Rb+ influxes differentiate between growth arrest of cells by different agents. 631 30

The effects of guanosine tetraphosphate (ppGpp) and pyrimidine ribonucleoside triphosphates on Escherichia coli aspartate transcarbamylase (ATCase) synthesis were examined. To determine the effect of ppGpp, a stringent (relA+) and relaxed (relA) isogenic pair of E. coli K-12 strains was starved for isoleucine, and the residual rate of synthesis of this enzyme was measured. It was necessary to starve the strains for uracil before the isoleucine limitation to maintain similar, low levels of UTP, the putative pyrimidine effector of ATCase synthesis. The isoleucine starvation of the stringent strain caused an immediate 10-fold increase in the intracellular concentration of ppGpp, which was coincident with the cessation of the synthesis of the enzyme. The elevated level of ppGpp then decayed until it reached an intracellular concentration similar to that found in unstarved cells. Enzyme synthesis resumed at this time. In the relaxed strain, the intracellular concentration of ppGpp did not increase upon isoleucine starvation and synthesis of the enzyme was not repressed. These experiments strongly indicated that ppGpp acts as a negative effector of ATCase synthesis. The repression of ATCase synthesis by ppGpp was demonstrated directly by using a Salmonella typhimurium (relA) in vitro coupled transcription-translation system with a lambda specialized transducing phage carrying the E. coli K-12 operon encoding the subunits of this enzyme (pyrBI) as a source of DNA. This in vitro system was also used to measure the effects of UTP and CTP on ATCase synthesis. Increasing the concentration of UTP in the in vitro reaction mixture resulted in strong repression of this synthesis, whereas increasing the CTP concentration did not affect synthesis significantly. Possible mechanisms for the regulation of pyr gene expression, including attenuation control, are discussed.
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PMID:Regulation of Escherichia coli aspartate transcarbamylase synthesis by guanosine tetraphosphate and pyrimidine ribonucleoside triphosphates. 633 30

The involvement of undermodified tRNA in the regulation of the ilvGEDA operon has been investigated using Escherichia coli C6, a relA-, Cys-, Met- mutant. This strain accumulates thionucleotide-deficient or methyl-deficient tRNA when starved for cysteine or methionine, respectively. The levels of threonine deaminase, the ilvA gene product, and transaminase B, the ilvE gene product, were both lower in cysteine-starved cells, as compared with either growing or methionine-starved cultures. When cysteine was added to cysteine-starved cells, growth ensued promptly and both enzyme activities returned to control levels. Treatment of recovering cultures with valine limited growth by isoleucine limitation, but did not cause a derepression of the ilvGEDA operon. Valine treatment of nonstarved or methionine-starved cells led to the expected increase in threonine deaminase and transaminase B activities. Cysteine-starved cells slowly regained the ability to derepress the operon after 3 h of recovery in complete medium. In contrast, the induction of the lac operon was normal in cysteine-starved cultures, even in the presence of valine. The loss of derepressibility of the ilvGEDA operon was correlated with the presence of a kinetically and chromatographically altered tRNAIle in cysteine-starved cells. No changes in tRNAIle were observed after methionine starvation. Using the periodate method, we found that the charging of tRNAIle increased from the normal level of 60 to 80% or greater after starvation for cysteine. Under conditions where the ilvGEDA operon was fully derepressed in nonstarved cells, the charging of tRNAIle fell to 27%. Unexpectedly, nearly identical results were obtained with cysteine-starved cells after an identical derepression test. These results suggest that factors other than the aminoacylation state of tRNAIle may be important in the regulation of this operon. In particular, modifications to tRNA which involve cysteine may be necessary for controlling the expression of the ilvGEDA operon in E. coli.
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PMID:Cysteine starvation, isoleucyl-tRNAIle, and the regulation of the ilvGEDA operon of Escherichia coli. 634 28

The effects of dietary protein level, exogenous insulin and starvation on amino acid (AA) uptake or release from the hindquarters of steers were studied. Irrespective of diet fed, physiologic state or time after feeding there was a net release of alanine and glutamine from hind limbs of steers. Steers from control 1 exhibited a net release of leucine, valine and isoleucine (branched-chain amino acids, BCAA) in the postabsorptive (prefeeding) state, but steers from control group 2 exhibited some BCAA uptake by the hind limb. At 2 and 4 hours postfeeding, there was marked net uptake by hind limbs of BCAA and total AA in steers fed the control (12.8% protein) diets. At 2 and 4 hours after feeding there was slight hind-limb uptake of BCAA and total AA in steers fed the low protein diet, while there was a massive uptake of BCAA and total AA by hind limbs of steers fed the high protein diet. Upon insulin injection to postabsorptive steers, BCAA and total AA uptake by hind limbs was markedly stimulated at 1 and 2 hours, but by 4 hours the AA flux pattern had reverted to that in the postabsorptive state. After 24 and 48 hours of starvation, steer hindquarters released significant quantities of BCAA, essential amino acids and total amino acids.
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PMID:Effect of nutritional state and insulin on hind-limb amino acid metabolism in steers. 634 21

Stringent and relaxed strains of E. coli subjected to isoleucine starvation were examined by follow-wing the incorporation of 3H-thymidine into chromosomal DNA. After valine treatment to trigger an isoleucine deprivation (p)ppGpp is synthesized in the stringent strain only. Remarkable differences in the morphology of the amino acid starved cells of the stringent and relaxed strains can be observed. Upon isoleucine limitation 3H-thymidine incorporation into DNA is reduced in both strains, but this inhibition is remarkably delayed in the relaxed strain. Our result show that the reduction of chromosomal DNA synthesis during amino acid limitation occurs also without ppGpp, but in the presence of ppGpp this process is accelerated.
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PMID:[3H-thymidine incorporation following isoleucine limitation in stringent and relaxed controlled strains of Escherichia coli]. 637 68

Normal volunteers were evaluated in the postabsorptive state, following 10 days of protein-calorie starvation, and during intravenous feeding ( ivf ) to determine the impact of nutritional status upon exertion-induced muscle amino acid metabolism. An isolated forearm model allowed an evaluation of recovery of metabolism following 1 min of submaximal isotonic exercise. Forearm blood flow returned to near basal levels within 15 min after exertion during postabsorptive and ivf conditions, but remained greater than or equal to 150% of basal at 1 hr after exercise during starvation. At 30 and 60 min after exercise, forearm plasma flux of total and essential amino acids were unchanged from basal in the postabsorptive state. However, the pattern of essential amino acid flux demonstrated a relative reduction in isoleucine and leucine efflux compared with basal, and this pattern persisted throughout 1 hr of recovery. During starvation, a significant (P less than 0.05) increase in total and essential amino acid efflux was observed throughout the recovery period. Starvation was also associated with significant increases in alanine and lysine efflux during recovery. Intravenous feeding was associated with a significant (P less than 0.05) uptake of essential amino acids with respect to basal levels at 30 min after exercise. At 60 min, there was a shift to total amino acid efflux but no change from basal flux for essential amino acids. During ivf , the pattern of essential amino acid uptake returned to basal within 1 hr after exertion.
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PMID:Influence of nutritional status on exertion-induced forearm amino acid metabolism in normal man. 642 22

Histone mRNA was partially purified from mouse myeloma cells synchronized in S phase by isoleucine starvation. A cDNA was prepared that contained sequences complementary to all five mouse histone genes. This cDNA was used to screen a library of mouse DNA in lambda phage. The positive clones were screened by hybridization with sea urchin histone gene-specific probes to identify those clones that contained histone genes. Confirmation of this identification was obtained by hybridization with Drosophila histone genes. Two independent clusters of histone genes were isolated. One, MM531, contains regions hybridizing specifically to H3, H4, and H1 and the other, MM221, contains two regions hybridizing specifically to H3 and single regions complementary to H4, H2b, and H2a. They are not part of a simple repeating structure. The nucleotide sequence of the coding region of the H3 gene in MM531 has been determined. This gene could code for a variant H3 protein that has several amino acid substitutions not reported in other H3 proteins.
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PMID:Isolation of two clusters of mouse histone genes. 645 99

The G1 blocks in three temperature-sensitive (ts) Syrian hamster cell-cycle mutants have been mapped in relation to other G1 landmarks. Two mutants reported here, ts-559 and ts-694, show defective progression only in G1. When shifted from the permissive temperature of 33 degrees C to the non-permissive temperature of 39 degrees C, G1 cells of these two mutants show no further cell cycle progression, while cells in S, G2 and mitosis progress through the cell cycle but become blocked after entering G1. The two mutants complement each other, and also complement the previously reported mutant ts-550C with blocks in both G1 and G2 of the cell cycle. The locations of the G1 blocks in both ts-559 and ts-694 are before the hydroxyurea arrest point. The G1 ts point in ts-694 is prior to the isoleucine deprivation and serum starvation points, while the G1 block in ts-559 is after the serum starvation point but before the isoleucine block. Other G1 block points which have been reported are in mutants of different species and isolated in different laboratories, causing difficulties for relative positioning of the blocks in G1. The mutants for mapping in this study have been isolated from the same cell line. The G1 ts arrest points of ts-559 and ts-694, and that found in ts-550C, together with nutritional deprivations and metabolic inhibitors, provide seven reference points which divide G1 into six segments, each of which is bracketed by two adjacent points: mitosis, ts-694 block, serum starvation arrest point, ts-559 block, isoleucine deprivation arrest point, ts-550C block, hydroxyurea or excess-thymidine arrest segment.
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PMID:Cell division cycle in mammalian cells. VIII. Mapping of G1 into six segments using temperature-sensitive cell cycle mutants. 649 47

We have studied the metabolism of dihydrofolate reductase (DHFR) RNA in cells synchronized in the G1 phase of the cell cycle by starvation for isoleucine and glutamine. The relative content and stability of DHFR mRNA and the relative rate of transcription of the DHFR gene are similar in starved and exponentially growing cells. However, the relative rate of labeling of DHFR mRNA is about three times lower in starved cells than in exponentially growing cells. When the starved cells are stimulated to reenter the cell cycle by feeding them with complete medium, the relative rate of labeling of DHFR mRNA increases about fourfold within 6 h. However, the relative rate of transcription of the DHFR gene changes very little during this period. Continuous labeling experiments show that starved cells convert DHFR heterogeneous nuclear RNA into cytoplasmic DHFR mRNA much more slowly than serum-limited or exponentially growing cells. Pulse-chase experiments show that DHFR mRNA sequences contained in DHFR heterogeneous nuclear RNA appear to be conserved in starved cells. In addition, the content of DHFR RNA sequences in the nuclei of starved cells is about three times greater than that in exponentially growing cells. Delayed processing of DHFR heterogeneous nuclear RNA is also observed when exponentially growing cells are treated with inhibitors of protein synthesis. Our results suggest that, although delayed processing leads to a decrease in the initial labeling rate of DHFR mRNA, it does not result in a decrease in the actual rate of production of the message.
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PMID:Delayed processing of dihydrofolate reductase heterogeneous nuclear RNA in amino acid-starved mouse fibroblasts. 664 25


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