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At least 919 records · Page 51Linked to original sources
PubMed2004

Global transcriptional analysis of the phosphate starvation response in Sinorhizobium meliloti strains 1021 and 2011.

The global response to phosphate starvation was analysed at the transcriptional level in two closely related strains of Sinorhizobium meliloti, Rm1021 and Rm2011. The Pho regulon is known to be induced by PhoB under conditions of phosphate limitation. Ninety-eight genes were found to be significantly induced (more than three-fold) in a phoB -dependent manner in phosphate-stressed cells, and phoB -independent repression of 86 genes was observed. Possible roles of these genes in the phosphate stress response are discussed. Twenty new putative PHO box sequences were identified in regions upstream of 17 of the transcriptional units that showed phoB -dependent, or partially phoB -dependent, regulation, indicating direct regulation of these genes by PhoB. Despite the overall similarity between the phosphate stress responses in Rm1021 and Rm2011, lower induction rates were found for a set of phoB -dependent genes in Rm1021. Moreover, Rm1021 exhibited moderate constitutive activation of 12 phosphate starvation-inducible, phoB -dependent genes when cells were grown in a complex medium. A 1-bp deletion was observed in the pstC ORF in Rm1021, which results in truncation of the protein product. This mutation is probably responsible for the expression of phosphate starvation-inducible genes in Rm1021 in the absence of phosphate stress.

ATP-Binding Cassette Transporters↗
PubMed1999

PhoB-dependent transcriptional activation of the iciA gene during starvation for phosphate in Escherichia coli.

The IciA protein from Escherichia coli has been shown specifically to inhibit the in vitro initiation of chromosomal DNA replication. However, the in vivo role of IciA has not yet been established. In order to investigate the in vivo function of this protein, expression of the iciA gene was studied by monitoring the beta-galactosidase activity specified by an iciA promoter-lacZ fusion inserted into the chromosome. Among the conditions tested (carbon starvation, the stringent response, phosphate starvation, and the SOS response), only phosphate depletion increased iciA expression. Supplementation of phosphate-depleted cultures with inorganic phosphate reduced the beta-galactosidase activity to basal levels. Enhanced expression of iciA-lacZ was dependent upon the PhoB protein. PhoB is known to be a transcriptional activator of the Pho regulon, expression of which is activated during phosphate starvation. It was also found that the iciA promoter contains a PhoB protein-binding sequence, termed the Pho box, which is necessary for the activation of genes of the Pho regulon. These results suggest that the iciA gene is a member of the Pho regulon.

Bacterial Proteins↗
PubMed2006

Effect of carbon starvation on toluene degradation activity by toluene monooxygenase-expressing bacteria.

Subsurface bacteria commonly exist in a starvation state with only periodic exposure to utilizable sources of carbon and energy. In this study, the effect of carbon starvation on aerobic toluene degradation was quantitatively evaluated with a selection of bacteria representing all the known toluene oxygenase enzyme pathways. For all the investigated strains, the rate of toluene biodegradation decreased exponentially with starvation time. First-order deactivation rate constants for TMO-expressing bacteria were approximately an order of magnitude greater than those for other oxygenase-expressing bacteria. When growth conditions (the type of growth substrate and the type and concentration of toluene oxygenase inducer) were varied in the cultures prior to the deactivation experiments, the rate of deactivation was not significantly affected, suggesting that the rate of deactivation is independent of previous substrate/inducer conditions. Because TMO-expressing bacteria are known to efficiently detoxify TCE in subsurface environments, these findings have significant implications for in situ TCE bioremediation, specifically for environments experiencing variable growth-substrate exposure conditions.

Biodegradation, Environmental↗
PubMed1978

Role of silicon on diatom metabolism. IX. Differential synthesis of DNA polymerases and DNA-binding proteins during silicate starvation and recovery in Cylindrotheca fusiformis.

During recovery from silicate-starvation, a period of active DNA synthesis, synchronized cells of Cylindrotheca fusiformis incorporated 3 times more L-[U-14C]aspartate than did starved cells. Of the diatoms's four DNA polymerases, A and D are synthesized during silicate recovery, indicating that they are involved in silicate-dependent DNA replication. Polymerase B, and the chloroplast enzyme, polymerase C, are synthesized during silicate-starvation and their levels are unaffected by the addition of silicate. DEAE-Sephadex analysis of the DNA-binding proteins, labeled with [14C]- and [3H]asparate, shows that only three proteins are synthesized in cells recovering from silicate-starvation. Two of these proteins correspond to polymerases A and D, while the function of the third protein is not known. At least 15 other proteins are present in silicate-starved cells and their synthesis is repressed upon the addition of silicate. Models are proposed which describe the modes by which silicate might regulate DNA synthesis in the diatom.

Amino Acids↗
PubMed1978

Polysome activity in relation to growth and protein starvation in brains and hearts of cultured early chick embryos.

In previous studies, brains but not hearts of intact early chick embryos were found to be sensitive to protein starvation. In this study, the in vitro protein synthetic activity of polysomes isolated from brains was found to be greater than those isolated from hearts. Starvation reduced the protein synthetic activity of polysomes in vitro but the extent of the reduction was approximately the same for both brains and hearts. A reduction in the amount of ribosomes as polysomes may have contributed to the lower synthetic activity of polysomes from tissues of starved embryos but not to the differences in synthetic activities between brains and hearts. In addition, neither the stability of isolated polysomes nor ribosome-associated ribonuclease activity appeared responsible for the differences observed in polysome synthetic activities. In direct relationship to the differential sensitivity of brains and hearts to starvation observed in the intact embryo, ribosomes isolated from brains of both growing and starved embryos were more readily degraded during in vitro incubation than those from hearts.

Animals↗
PubMed1979

The effect of magnesium starvation on the dissociation of ribosomal proteins from Escherichia coli K-12 ribosomes.

The effect of magnesium starvation upon the fate of individual ribosomal proteins was studied in Escherichia coli. During a 21 h incubation in the absence of Mg2+ the 30 S subunit was more susceptible to degradation, retaining an average 31.9% of its ribosomal proteins as compared to 40.0% for the 50 S subunit. An examination of those 50-S proteins dissociated to a lesser extent than the average value (L1, L2, L3, L7, L10, L13, L16, L17, L19, L21, L22, L23, and L29) revealed that, with the exception of L16, all were classified by Dohme and Nierhaus [5] as tightly bound. Of the ribosomal proteins dissocated during magnesium starvation only five were reincorporated (and these to a minimal degree) during recovery of cells in a medium containing Mg2+. These studies suggest that ribosomal proteins once released from the ribosome particles during magnesium starvation are not reutilized in the assembly of new subunits.

Bacterial Proteins↗
PubMed1986

Glucose starvation alters insulin but not IGF-I binding to Chinese hamster ovary (CHO) cells.

The pattern of cellular protein glycosylation can be altered in CHO cells by glucose starvation. When wild type CHO cells are deprived of glucose, 125I-insulin binding increases from a B/F of 0.033 +/- 0.004 to 0.063 +/- 0.011, due to an increase in receptor affinity. The already elevated insulin binding to mutant B4-2-1 CHO cells, whose genetic defect causes abnormal glycosylation mimicking the pattern seen in the glucose starved normal cells, is not affected by glucose starvation. In neither cell line is 125I-IGF-I binding affected by glucose starvation. These data support the hypothesis that abnormal glycosylation can alter insulin binding to its receptor. Furthermore, there is a striking difference in the susceptibility of IGF-I and insulin receptors to alterations in glycosylation.

Animals↗
PubMed1984

Selective inhibition of calcium-stimulated cation-induced pinocytosis by starvation and inhibitors of protein synthesis in Amoeba proteus.

The capacity of Amoeba proteus to form pinocytotic channels after pretreatment with either puromycin, cycloheximide, emetine or a long period of starvation was studied. The effect on pinocytosis of the three inhibitors of protein synthesis was similar. They preferentially affected pinocytosis induced by Na+ with little effect on K+-induced pinocytosis. In Ca2+-deficient media, Na+-induced pinocytosis was inhibited, while the addition of Ca2+ restored channel formation. The degree of inhibition of Na+-induced pinocytosis was influenced by the concentration of Ca2+ in the inducing solution. Selective Ca2+-reversible inhibition of Na+-induced pinocytosis also occurred after starvation or treatment with a proteolytic enzyme, subtilisin. The membrane potential in starved or emetine-treated cells in culture medium was normal and their depolarising response to inducers was not diminished in solutions containing Na+. The resting input resistance of these cells was higher than in normal amoebae, but no significant difference in electrical parameters was observed after pinocytosis was induced. It is suggested that starvation, inhibition of protein synthesis, and enzyme digestion deplete the membrane of structures which are necessary for normal Ca2+ functions during induction of pinocytosis by Na+-like inducers.

Amoeba↗
PubMed1991

Pathological effects of Blastocrithidia triatomae (Trypanosomatidae) on the reduviid bug Triatoma infestans after infection by membrane feeding and long-term starvation.

Developmental time and mortality in larvae of the reduviid bug Triatoma infestans were studied in uninfected groups and in those infected with Blastocrithidia triatomnae by in vitro feeding with 10(4) cyst stages/cm(3) blood. Bugs were subsequently subjected to two different starvation periods. In bugs fed at weekly intervals infection with B. triatomae was associated with developmental retardation, increasing in the final instars, and with increased mortality in the third and preadult instar. Compared to these groups, long-term starvation caused slightly lower mortality rates of uninfected groups and in infected bugs a remarkably higher mortality rate in the preadult instar. Total mortality rates of infected groups were nearly unaffected by starvation.

Animals↗
PubMed1986

The effect of starvation on skeletal muscle function in man.

Measuring skeletal muscle function may be a diagnostic aid to detect malnutrition. To evaluate this hypothesis 11 lean women were studied before and after 5 days of total starvation. Skeletal muscle function was assessed as hand grip strength and as adductor pollicis muscle function after electrical stimulation of the ulnar nerve. The muscle function variables were force of contraction at 5, 10, 20 and 50 Hz stimulation, relaxation rate and endurance. In addition some currently used anthropometric and biochemical nutritional indices were serially determined. Hand grip strength was decreased (p < 0.05) and the function of the adductor pollicis muscle was altered with a higher contraction force at 10 Hz (p < 0.01), a slower relaxation rate (p < 0.05) and a reduced endurance (p < 0.05). These changes were all within the normal ranges. Triceps skin fold and arm muscle circumference were not changed after a mean weight loss of 3.3 kg (p < 0.05). However blood glucose, insulin and triiodothyronine all decreased (p < 0.01) indicating a metabolic adaptation to starvation. Prealbumin (p < 0.05) and fibronectin (p < 0.01) were also lowered. In conclusion, skeletal muscle function was significantly altered after five days of total starvation. However, to identify short term nutritional depletion in clinical practice the changes in muscle function were too small to be diagnostically useful.

Journal Article↗
PubMed1986

Starvation induced changes in quantitative measures of liver function in the rat.

Liver function was estimated quantitatively as the capacity of urea-N synthesis (CUNS), the galactose elimination capacity (GEC) and the antipyrine plasma clearance (APC) in rats following 24, 48, and 96 h of food deprivation. CUNS rose to a maximum following 24 h of starvation, then decreased to the control value at 48, 72, and 96 h (p = 0.02). GEC decreased following starvation, significant so at 48 h (p = 0.02). APC decreased at 48, and 72 h (p = 0.01), but rose to the control value at 96 h. It is concluded that a precise standardisation of starvation is important for interpretation of minor changes in CUNS, GEC, and APC.

Journal Article↗
PubMed1995

Self-starvation in context: towards a culturally sensitive understanding of anorexia nervosa.

Extreme forms of self-starvation can be traced across time and place, and may be construed using a variety of explanatory models. Curiously, the prevailing biomedical definition of anorexia nervosa has assigned primacy to the exclusive use of 'fat phobia' by the affected subjects to justify their diminished food intake. This paper assembles evidence to show that this culturally constructed version of fat phobic anorexia nervosa has neglected the full metaphorical significance of self-starvation and, when applied in a cross-cultural context, may constitute a category fallacy. By delegitimizing other rationales for non-eating and thereby barring subjective expressions, this regnant interpretive strategy may obscure clinicians' understanding of patients' lived experience, and even jeopardize their treatment. Nonetheless, it is a relatively simple task to attune the extant diagnostic criteria to a polythetic approach which will avert cultural parochialism in psychiatric theory and practice. As a corollary of the archival and ethnocultural study of extreme self-starvation, there is, contrary to epistemological assumptions embedded in the biomedical culture of contemporary psychiatry, no 'core psychopathology' of anorexia nervosa.

Adult↗
PubMed1987

Effect of protein starvation on protein turnover in liver, oviduct and whole body of laying hens.

1. Whole body protein turnover rates in White Leghorn laying hens were reduced by protein starvation for 7 days, followed by complete restoration by protein repletion for 7 days. 2. Protein starvation considerably reduced fractional and absolute rates of protein synthesis both in the liver and, to a greater extent, in the oviduct. 3. It was suggested that a considerable portion of the reduced whole body protein synthesis could be accounted for by the reduced protein synthesis in these organs when laying hens were subjected to protein starvation.

Animals↗
PubMed1991

Expression in Caulobacter crescentus of the phosphate-starvation-inducible porin OprP of Pseudomonas aeruginosa.

The gene for the phosphate-starvation-inducible outer membrane protein OprP, of Pseudomonas aeruginosa was introduced into Caulobacter crescentus CB2A on a plasmid vector. As is the case in P. aeruginosa and Escherichia coli the oprP gene was inducible under conditions of limiting phosphate in C. crescentus. However, the maximal medium concentration of phosphate which still permitted induction of OprP was lower in C. crescentus (50 microM) than in P. aeruginosa (200 microM). Induction of OprP was coincident with the process of stalk elongation, known to occur in C. crescentus under phosphate starvation conditions. When induced, OprP was localized to the cell envelope and became a major membrane protein, indicating that the Pseudomonas promoter was efficiently recognized in C. crescentus and that the gene product was targeted to the appropriate region of the cell. Our data provide support for the hypothesis that the mechanism for regulation of phosphate-starvation-inducible genes is highly conserved amongst the eubacteria.

Bacteria↗
PubMed1993

Effects of starvation on the urinary contents of primary thromboxane and prostacyclin metabolites and a possible selenium-dependent role of prostacyclin in the renal handling of ketone bodies.

The aim of this study was to investigate whether urinary prostanoids, as an index of renal synthesis of these compounds, are affected in selenium (Se) deficiency and, if so, whether such changes could add to our understanding of the high excretion of ketone bodies in Se-deficient rats (p < 0.005 vs Se-adequate rats). Male rats were fed a Se-deficient diet with less than 0.01 mg Se/kg or the same diet supplemented with 0.2 mg Se/kg. The urinary contents of prostaglandin E2 (PGE2), PGF2 alpha and 6-keto PGF1 alpha were not significantly affected by the Se status. However, there was a positive correlation between the urinary contents of ketone bodies and 6-keto PGF1 alpha in Se deficiency (with p < 0.02 for acetaoacetate and p < 0.05 for 3-hydroxybutyrate). In contrast, only negative (nonsignificant) relationships were observed between these same parameters in Se-adequate rats. No correlations between urinary contents of ketone bodies and PGE2, PGF2 alpha or thromboxane B2 (TXB2) were obtained. Compared to fed rats, starvation caused a 4-fold increase in the urinary TXB2 content in Se-adequate, as well as in Se-deficient rats (p < 0.001). Starvation had an opposite effect on the content of 6-keto PGF1 alpha, which decreased (to 64% that of fed animals p < 0.001) in Se-adequate rats and, nonsignificantly (to 93% that of fed animals) in the Se-deficient group. It is concluded that starvation profoundly affects the urinary contents (and thus, probably renal synthesis) of TX and prostacycline (PGI2).(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed2005

Qualitative simulation of the carbon starvation response in Escherichia coli.

In case of nutritional stress, like carbon starvation, Escherichia coli cells abandon their exponential-growth state to enter a more resistant, non-growth state called stationary phase. This growth-phase transition is controlled by a genetic regulatory network integrating various environmental signals. Although E. coli is a paradigm of the bacterial world, it is little understood how its response to carbon starvation conditions emerges from the interactions between the different components of the regulatory network. Using a qualitative method that is able to overcome the current lack of quantitative data on kinetic parameters and molecular concentrations, we model the carbon starvation response network and simulate the response of E. coli cells to carbon deprivation. This allows us to identify essential features of the transition between exponential and stationary phase and to make new predictions on the qualitative system behavior following a carbon upshift.

Carbon↗
PubMed2004

Effects of fungal food quality and starvation on the fatty acid composition of Protaphorura fimata (Collembola).

The lipid pattern of animals is influenced by species, life stage, environmental conditions and diet. We investigated the effects of food quality and starvation on the phospholipid (PLFA) and neutral lipid (NLFA) fatty acid pattern of the collembolan Protaphorura fimata. Collembolans were fed with two common soil fungi, Agrocybe gibberosa and Chaetomium globosum, of which the cellular lipid composition was analysed. A. gibberosa was grown on agar with different nitrogen contents, resulting in altered fatty acid patterns and C:N ratios, i.e. fungi of different food quality. Collembolans did not mirror the lipid composition of the fungal diet as the pattern of major NLFAs in P. fimata was vice versa. Presumably, altered food quality of fungi caused compensatory responses by the collembolans, thereby diminishing the fungal signal. In a further experiment P. fimata (previously maintained with C. globosum) was kept without food for up to 4 weeks. Starvation resulted in a decline in the total amount of NLFAs; however, it did not affect the fatty acid pattern, indicating that NLFAs were degraded indiscriminately. Generally, the PLFA profile of the collembolans changed only slightly due to variations in diet quality or starvation.

Fatty Acids↗
PubMed2004

Role and regulation of starvation-induced autophagy in the Drosophila fat body.

In response to starvation, eukaryotic cells recover nutrients through autophagy, a lysosomal-mediated process of cytoplasmic degradation. Autophagy is known to be inhibited by TOR signaling, but the mechanisms of autophagy regulation and its role in TOR-mediated cell growth are unclear. Here, we show that signaling through TOR and its upstream regulators PI3K and Rheb is necessary and sufficient to suppress starvation-induced autophagy in the Drosophila fat body. In contrast, TOR's downstream effector S6K promotes rather than suppresses autophagy, suggesting S6K downregulation may limit autophagy during extended starvation. Despite the catabolic potential of autophagy, disruption of conserved components of the autophagic machinery, including ATG1 and ATG5, does not restore growth to TOR mutant cells. Instead, inhibition of autophagy enhances TOR mutant phenotypes, including reduced cell size, growth rate, and survival. Thus, in cells lacking TOR, autophagy plays a protective role that is dominant over its potential role as a growth suppressor.

Animals↗