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

Heat-resistant derivatives of a Bacillus subtilis 168 strain carrying an xhi mutation, which causes heat-sensitive induction of the PBSX prophage, have been isolated and screened for the acquisition of auxotrophy. Two classes of auxotrophs were isolated, namely Pro- and Pro-Met-; they lacked the ability to produce PBSX, as shown by their resistance to mitomycin C-induced lysis. The proline and methionine requirements and the resistance to mitomycin C were shown to segregate together in phage PBS1-mediated transduction crosses and to be linked to thiB, which is known to be co-transducible with the PBSX prophage. It was therefore proposed that these strains had deletions which removed all or part of the PBSX prophage together with adjacent bacterial DNA encoding the pro(AB) and metC genes. The met mutation was shown to be metC in PBS1 transduction crosses; this gene is known to be co-transducible with the PBSX prophage. The proline requirement was probably due to the deletion of a pro gene which was demonstrated to lie between the PBSX prophage and metC and which was 90% co-transducible with metC. These deletions have been transduced into a strain which was cured of phage SP beta, another bacteriophage carried by B. subtilis 168. No phage particles could be seen in mitomycin C-induced cultures of such strains. The PBSX-deletion strains grew with the same generation time as the PBSX+ parent in L-broth (27 min at 35 degrees C) but they were slower in minimal medium (e.g. 72 min as against 51 min in the PBSX+ strain). Besides being resistant to mitomycin C-induced lysis, the deletion strains were also resistant to lysis induced by thymine starvation of thymine auxotrophs and the loss of viability of these strains after thymine starvation was 100-fold less than in the PBSX+ parent. The deletion strains had not, however, lost the bacterial autolytic enzymes, since they were still susceptible to lysis when placed under semi-anaerobic conditions.
 ...
PMID:Selection of Bacillus subtilis 168 mutants with deletions of the PBSX prophage. 677 36

Subcutaneous administration of insulin(10 U/kg) produced hypoglycemia in rats with a concomitant induction of feeding. The opiate antagonist naloxone failed to alter food ingestion following insulin administration when quantitated over a 3-hour period; however, naloxone (20 mg/kg) significantly suppressed eating during the first hour of the study. Starvation-induced feeding was markedly suppressed by relatively low doses of naloxone (1 mg/kg). The dopamine antagonist haloperidol, the cholinergic antagonist atropine, and the putative satiety factors CCK-8, bombesin, histidyl-proline diketopiperazine and calcitonin suppressed insulin-induced feeding. Naloxone, CCK-8 and bombesin significantly raised blood glucose levels following insulin induced hypoglycemia.
 ...
PMID:Peptidergic control of insulin-induced feeding. 702 93

CHO-K1 requires proline for growth. Two proline-independent revertants were isolated--K1-J and K1-6. CHO-K1 pro- is much more sensitive than the pro+ cell lines to inhibition of growth by addition to the medium of amino acids and amino acid analogues that are transported through the A system. In contrast, pro+ cells are as sensitive as, or in some cases slightly more sensitive than, pro- cells to glycine, basic amino acids, and to amino acids that are mainly transported by the L system. The A system analogue alpha(methylamino) isobutyric acid (MAIB) in low concentrations reacts competitively with proline to regulate the growth of pro- cells, yielding a Ki for MAIB of 0.56 mM. CHO-K1 and K1-6 transport proline at the same initial rate and are equally sensitive to the inhibition of proline transport by alanine. Alanine and MAIB inhibit proline transport strongly and similarly in CHO-K1. Thus although these compounds inhibit the transport of proline by both cell types to the same extent, pro+ cells are immune to the effect of this starvation since they are able to synthesize their own proline. We also describe a secondary inhibition caused by high A system amino acid concentrations that affects both pro- and pro+ cells.
 ...
PMID:Inhibition of growth of proline-requiring Chinese hamster ovary cells (CHO-k1) resulting from antagonism by a system amino acids. 719 46

Histidyl-proline diketopiperazine was found to suppress food intake during stress-induced eating (10(-6)--10(-8) mol), starvation-induced eating (10(-8) mol) and over an 8 h period of spontaneous eating (10(-8) mol). In contrast, other cyclic piperazines failed to alter food ingestion. The suppressive effect of histidyl-proline diketopiperazine was antagonized by the enkephalin analogue, D-Ala-Met-enkephalin, in equimolar concentrations.
 ...
PMID:Histidyl-proline diketopiperazine decreases food intake in rats. 719 19

Rat hepatoma cells accumulate considerably less 2-aminoisobutyrate after cultivating in the absence of serum--the change in rate of aminoisobutyrate uptake takes place within 1 h of serum starvation. Starvation of amino acids by contrast raises aminoisobutyrate uptake in the presence or absence of serum, but the cells are much less responsive to amino acid supply than to availability of serum. Phosphate (10 mM) reduced aminoisobutyrate uptake by cells grown in serum to that exhibited by serum-starved cells. Aminoisobutyrate uptake by cells grown in serum was reduced by glycine, proline, alanine, serine, glutamine, methylaminoisobutyrate and 2-aminonorbornane-2-carboxylate, the effects of methylaminoisobutyrate and 2-aminonorbornane-2-carboxylate being additive. However, similar inhibition phenomena were not seen for cells deprived of serum where aminoisobutyrate uptake tended to a relatively constant level insensitive to inhibitory influences, yet substantially greater than that arising by simple diffusion. The comparative insensitivity of our hepatoma line when starved of serum to competition and repression phenomena is in contrast to findings of others. Our results also suggest a lack of clear delineation of specificities for the A and L transport systems as usually defined.
 ...
PMID:Influence of serum and amino acids on the accumulation of aminoisobutyrate by rat hepatoma cells. A dedifferentiation of transport routes? 730 45

Regulation of A system amino acid transport was studied in primary cultures of the R3230AC mammary adenocarcinoma. Higher rates of carrier-mediated Na+-dependent proline transport, vc, was decreased and was attributed to a two-fold decrease in Vmax and a two-fold increase in Km. When compared to cells grown in standard media (Eagle's minimal essential medium, MEM), cells grown in media supplemented with A system substrates (alanine, serine, glycine, and proline) demonstrated adaptive decreases in proline transport; the decrease was due to two-fold reduction in Vmax, with no change in Km for proline. Even in the presence of preferred substrates for the A system, a density-dependent decrease in proline transport was manifested. Both fast- and slow-growing cultures maintained in MEM exhibited rapid increases in proline transport when switched to buffers devoid of amino acids; two-fold increases in Vmax were seen within 4 hr, but Km was unchanged. This starvation-induced adaptation was completely prevented by inclusion in the buffer of 10 mM proline, 0.1 mM alpha-(methylamino)-isobutyric acid (MetAIB) or 10 mM serine, whereas inclusion of the poorer A system substrate, phenylalanine (10 mM), had no effect. The effects of MetAIB to prevent starvation-induced increases in proline transport were dose-related, rapid, and reversible. Amino acid starvation-induced increases in proline transport were partially blocked by cycloheximide or actinomycin D. Data were obtained demonstrating a temporal relationship between increasing intracellular [proline] and decreasing vc for proline uptake. In addition, efflux of proline from preloaded cells preceded the increase in initial rates of proline entry. Taken together, we concluded that: 1) A system transport in primary cultures of this mammary adenocarcinoma is regulated by cell density as well as by availability of A system substrates, but these two types of regulation are kinetically distinct; and 2) starvation-induced enhancement of proline transport appears to be due to release from transinhibition, but may also involve a derepression-repression type of mechanism.
 ...
PMID:Influence of proliferative rates and A system substrate availability on proline transport in primary cell cultures of the R3230AC mammary tumor. 746 29

delta 1-pyrroline-5-carboxylate reductase (P5CR; [L-proline: NAD(P+) 5-oxidoreductase]; EC 1.5.1.2) catalyzes the final step in proline biosynthesis. We have shown that the proline-1 (pro-1) locus of Neurospora crassa encodes P5CR. The pro-1 gene was localized to a 3.2 kb region by complementation of (restoration of proline-independent growth to) a proline auxotroph carrying a recessive mutation at the pro-1 locus. The nucleotide sequence of this 3.2 kb region contains an open reading frame with coding capacity of 311 amino acids. The deduced polypeptide shows significant similarity to P5CR amino acid sequences. Similarity of N. crassa P5CR is greatest to that of the yeast, Saccharomyces cerevisiae, but is also strong to P5CR sequences from archaea, eubacteria, plants, and humans. In N. crassa, amino acid imbalance, including deficiency or excess of a single amino acid, such as histidine, induces expression of many amino acid biosynthetic genes that are under cross-pathway control, a general regulatory system analogous to general amino acid control in Saccharomyces. Although P5CR catalyzes the only committed step in proline biosynthesis, pro-1 expression was unaltered by histidine starvation and independent of CPC1, a positively acting transcription factor that mediates cross-pathway control in N. crassa.
 ...
PMID:Molecular characterization of the proline-1 (pro-1) locus of Neurospora crassa, which encodes delta 1-pyrroline-5-carboxylate reductase. 756 96

Saccharomyces cerevisiae wine-producing yeast cultures grown under model winemaking conditions could be induced to liberate hydrogen sulfide (H2S) by starvation for assimilable nitrogen. The amount of H2S produced was dependent on the yeast strain, the sulfur precursor compound, the culture growth rate, and the activity of the sulfite reductase enzyme (EC 1.8.1.2) immediately before nitrogen depletion. Increased H2S formation relative to its utilization by metabolism was not a consequence of a de novo synthesis of sulfite reductase. The greatest amount of H2S was produced when nitrogen became depleted during the exponential phase of growth or during growth on amino acids capable of supporting short doubling times. Both sulfate and sulfite were able to act as substrates for the generation of H2S in the absence of assimilable nitrogen; however, sulfate reduction was tightly regulated, leading to limited H2S liberation, whereas sulfite reduction appeared to be uncontrolled. In addition to ammonium, most amino acids were able to suppress the liberation of excess H2S when added as sole sources of nitrogen, particularly for one of the strains studied. Cysteine was the most notable exception, inducing the liberation of H2S at levels exceeding that of the nitrogen-depleted control. Threonine and proline also proved to be poor substitutes for ammonium. These data suggest that any compound that can efficiently generate sulfide-binding nitrogenous precursors of organic sulfur compounds will prevent the liberation of excess H2S.
 ...
PMID:Regulation of hydrogen sulfide liberation in wine-producing Saccharomyces cerevisiae strains by assimilable nitrogen. 757 81

Selection-induced mutations, sometimes called "directed," "adaptive," or "Cairnsian" mutations, are spontaneous mutations that occur as specific responses to environmental challenges, usually during periods of prolonged stress, and that occur more often when they are selectively advantageous than when they are selectively neutral. In this study I show that lesions in uvrA, uvrB, uvrC, or uvrD increase the mutation rate from trpA46 to trpA+ by 10(2)- to 10(4)-fold during tryptophan starvation, but those same lesions do not affect random mutation rates in growing cells when tryptophan is present. The increased selection-induced mutation rates remain specific to the gene that is under selection in that no increase in the mutation rate from trpA46 to trpA+ is detected during proline starvation. Evidence is presented showing that proline starvation produces a state of cellular stress which results in a burst of mutations from trpA46 to trpA+ when proline-starved cells are plated onto medium lacking tryptophan but containing proline. These results are consistent with the hypermutable state model for selection-induced mutagenesis.
 ...
PMID:Genetics of selection-induced mutations: I. uvrA, uvrB, uvrC, and uvrD are selection-induced specific mutator loci. 771 15

The Myxococcus xanthus asgA gene is one of three known genes necessary for the production of extracellular A-signal, a cell density signal required early in fruiting body development. We determined the DNA sequence of asgA. The deduced 385-amino-acid sequence of AsgA was found to contain two domains: one homologous to the receiver domain of response regulators and the other homologous to the transmitter domain of histidine protein kinases. A kanamycin resistance (Kmr) gene was inserted at various positions within or near the asgA gene to determine the null phenotype. Those strains with the Kmr gene inserted upstream or downstream of asgA are able to form fruiting bodies, while strains containing the Kmr gene inserted within asgA fail to develop. The nature and location of the asgA476 mutation were determined. This mutation causes a leucine-to-proline substitution within a conserved stretch of hydrophobic residues in the N-terminal receiver domain. Cells containing the insertion within asgA and cells containing the asgA476 substitution have similar phenotypes with respect to development, colony color, and expression of an asg-dependent gene. An analysis of expression of a translational asgA-lacZ fusion confirms that asgA is expressed during growth and early development. Finally, we propose that AsgA functions within a signal transduction pathway that is required to sense starvation and to respond with the production of extracellular A-signal.
 ...
PMID:The Myxococcus xanthus asgA gene encodes a novel signal transduction protein required for multicellular development. 772 94


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>