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PubMed1994

The time since castration influences the effects of short-term starvation on gonadotrophin secretion in male rats.

Short-term starvation suppresses the pituitary-testicular function in rats, evidently through inhibition of gonadotrophin-releasing hormone (GnRH) release. However, when gonadotrophin secretion is strongly enhanced, e.g. after castration, starvation does not suppress gonadotrophins. To test whether the time since castration affects the pituitary response to starvation, adult male rats were totally deprived of food for five days (only water allowed) immediately (acute castration) or two weeks after castration (chronic castration). The pituitary contents of GnRH receptors were decreased by starvation in sham-operated animals, unaffected in acutely castrated rats, but increased in chronically castrated animals, in comparison with appropriate controls (P < 0.01). Castration per se increased steady-state mRNA levels of the common alpha-chain and the LH and FSH beta-chains in all groups studied. The only consistent effect of starvation on these parameters was the 1.7 to 2-fold increase in the pituitary content of LH beta-subunit mRNA in acutely and chronically castrated rats (P < 0.01). Starvation alone suppressed LH secretion, acute castration eliminated this effect, but in chronically castrated rats, the starvation effect was stimulatory. Starvation did not affect FSH secretion in sham-operated and acutely castrated rats, but after chronic castration, the effect was stimulatory. In conclusion, the overall effect of starvation on gonadotrophins shifts gradually after castration from suppression, in sham-operated rats, to stimulation, in chronically castrated animals. Parallel changes in pituitary GnRH receptors suggest similar changes in GnRH secretion. Hence, starvation has both negative and positive effects on the GnRH-gonadotrophin-axis. The negative effect is evidently androgen-dependent and dominates in testes-intact animals. After chronic castration, only the positive, non-androgen dependent, stimulatory effect remains.

Animals↗
PubMed2001

A conserved MYB transcription factor involved in phosphate starvation signaling both in vascular plants and in unicellular algae.

Plants have evolved a number of adaptive responses to cope with growth in conditions of limited phosphate (Pi) supply involving biochemical, metabolic, and developmental changes. We prepared an EMS-mutagenized M(2) population of an Arabidopsis thaliana transgenic line harboring a reporter gene specifically responsive to Pi starvation (AtIPS1::GUS), and screened for mutants altered in Pi starvation regulation. One of the mutants, phr1 (phosphate starvation response 1), displayed reduced response of AtIPS1::GUS to Pi starvation, and also had a broad range of Pi starvation responses impaired, including the responsiveness of various other Pi starvation-induced genes and metabolic responses, such as the increase in anthocyanin accumulation. PHR1 was positionally cloned and shown be related to the PHOSPHORUS STARVATION RESPONSE 1 (PSR1) gene from Chlamydomonas reinhardtii. A GFP::PHR1 protein fusion was localized in the nucleus independently of Pi status, as is the case for PSR1. PHR1 is expressed in Pi sufficient conditions and, in contrast to PSR1, is only weakly responsive to Pi starvation. PHR1, PSR1, and other members of the protein family share a MYB domain and a predicted coiled-coil (CC) domain, defining a subtype within the MYB superfamily, the MYB-CC family. Therefore, PHR1 was found to bind as a dimer to an imperfect palindromic sequence. PHR1-binding sequences are present in the promoter of Pi starvation-responsive structural genes, indicating that this protein acts downstream in the Pi starvation signaling pathway.

Alleles↗
PubMed2003

Phosphate starvation triggers distinct alterations of genome expression in Arabidopsis roots and leaves.

Arabidopsis genome expression pattern changes in response to phosphate (Pi) starvation were examined during a 3-d period after removal of Pi from the growth medium. Available Pi concentration was decreased after the first 24 h of Pi starvation in roots by about 22%, followed by a slow recovery during the 2nd and 3rd d after Pi starvation, but no significant change was observed in leaves within the 3 d of Pi starvation. Microarray analysis revealed that more than 1,800 of the 6,172 genes present in the array were regulated by 2-fold or more within 72 h from the onset of Pi starvation. Analysis of these Pi starvation-responsive genes shows that they belong to wide range of functional categories. Many genes for photosynthesis and nitrogen assimilation were down-regulated. A complex set of metabolic adaptations appears to occur during Pi starvation. More than 100 genes each for transcription factors and cell-signaling proteins were regulated in response to Pi starvation, implying major regulatory changes in cellular growth and development. A significant fraction of those regulatory genes exhibited distinct or even contrasting expression in leaves and roots in response to Pi starvation, supporting the idea that distinct Pi starvation response strategies are used for different plant organs in response to a shortage of Pi in the growth medium.

Arabidopsis↗
PubMed1990

Starvation-specific formation of a peripheral exopolysaccharide by a marine Pseudomonas sp., strain S9.

The marine bacterium Pseudomonas sp. strain S9 produces exopolysaccharides (EPS) during both growth and total energy source and nutrient starvation. Transmission electron microscopy of immunogold-labeled cells demonstrated that the EPS is closely associated with the cell surface during growth (integral EPS), while both the integral form and a loosely associated extracellular (peripheral) form were observed during starvation. Formation and release of the latter rendered the starvation medium viscous. In addition, after 3 h of starvation in static conditions, less than 5% of the cells were motile, compared with 100% at the onset of starvation and approximately 80% subsequent to release of the peripheral EPS at 27 h of starvation. Inhibition of protein synthesis with chloramphenicol added before 3 h of starvation caused no increase in viscosity. However, addition of chloramphenicol at 3 h did not prevent the subsequent increase in viscosity displayed by S9 cells. The amount of integral EPS increased for both nontreated and chloramphenicol-treated S9 cells during the first hour of starvation, with a subsequent equal decrease. The chloramphenicol-treated cells, as well as cells of a transposon-generated mutant strain deficient in peripheral EPS formation, remained adhesive to a hydrophobic inanimate surface during the initial 5 h of starvation, whereas nontreated wild-type cells had progressively decreased adhesion capacity. During the initial 5 h of starvation, most of the nontreated cells but only a small fraction of the chloramphenicol-treated and mutant cells detached from the hydrophobic substratum.(ABSTRACT TRUNCATED AT 250 WORDS)

Bacterial Proteins↗
PubMed1993

Role of Clp protease subunits in degradation of carbon starvation proteins in Escherichia coli.

When deprived of a carbon source, Escherichia coli induces the synthesis of a group of carbon starvation proteins. The degradation of proteins labeled during starvation was found to be an energy-dependent process which was inhibited by the addition of KCN and accelerated when cells were resupplied with a carbon source. The degradation of the starvation proteins did not require the ATP-dependent Lon protease or the energy-independent proteases protease I, protease IV, OmpT, and DegP. During starvation, mutants lacking either the ClpA or ClpP subunit of the ATP-dependent Clp protease showed a partial reduction in the degradation of starvation proteins. Strains lacking ClpP failed to increase degradation of starvation proteins when glucose was added to starving cells. The clpP mutants showed a competitive disadvantage compared with wild-type cells when exposed to repeated cycles of carbon starvation and growth. Surprisingly, the glucose-stimulated, ClpP-dependent degradation of starvation proteins did not require either the ClpA or ClpB protein. The patterns of synthesis of starvation proteins were similar in clpP+ and clpP cells. The clpP mutants had reduced rates of degradation of certain starvation proteins in the membrane fraction when a carbon source was resupplied to the starved cells.

ATP-Dependent Proteases↗
PubMed1967

Magnesium starvation of Aerobacter aerogenes. 3. Protein metabolism.

The metabolism of the ribosomal and soluble protein components of Aerobacter aerogenes was examined during its incubation in a Mg(++)-deficient medium. Bacteria were exposed to leucine-H(3) during the exponential growth period preceding Mg(++) starvation, and extracts were prepared after intervals of starvation and were centrifuged through gradients of sucrose to separate ribosomal from soluble proteins. Ribosomal proteins synthesized during the preceding exponential growth were slowly lost from the ribosomes; after 8 hr of starvation, few, if any, sedimented with ribosomes. Losses of total protein, together with the known rate of ribosome decay during Mg(++) starvation, suggested that these ribosomal proteins are ultimately degraded to acid-soluble products and account for all protein lost by the starving cells. These conclusions were supported by studies of Mg(++) starvation in a uracil-requiring strain of A. aerogenes: during uracil starvation a smaller fraction of the proteins synthesized were ribosomal, and the fraction of protein which subsequently decayed during Mg(++) starvation was correspondingly less. During recovery from Mg(++) starvation, proteins, lost from disintegrated ribosomes, were not detectably reutilized into new particles even before their degradation to acid-soluble products was complete. Synthesis of soluble proteins continued for more than 24 hr of starvation at a rate per milliliter close to 45% of the instantaneous rate per milliliter of the exponentially growing bacteria at the time Mg(++) was removed. This value agreed with that found previously for synthetic rates of deoxyribonucleic acid, transfer ribonucleic acid, and ribosomal ribonucleic acid during starvation relative to rates during exponential growth.

Bacterial Proteins↗
PubMed1977

Derepression of amino acid transport by amino acid starvation in rat hepatoma cells.

Amino acid starvation causes an adaptive increase in the initial rate of transport of selected neutral amino acids in an established line of rat hepatoma cells in tissue culture. After a lag of 30 min, the initial rate of transport of alpha-aminoisobutyric acid (AIB) increases to a maximum after 4 to 6 h starvation of 2 to 3 times that seen in control cells. The increased rate of transport is accompanied by an increase in the Vmax and a modest decrease in the Km for this transport system, and is reversed by readdition of amino acids. The enhancement is specific for amino acids transported by the A or alanine-preferring system (AIB, glycine, proline); uptake of amino acids transported by the L or leucine-preferring system (threonine, phenylalanine, tyrosine, leucine) or the Ly+ system for dibasci amino acids (lysine) is decreased under these conditions. Amino acids which compete with AIB for transport also prevent the starvation-induced increase in AIB transport; amino acids which do not compete fail to prevent the enhancement. Paradoxically threonine, phenylalanine, tryptophan, and tyrosine, which do not compete with AIB for transport, block the enhancement of transport upon amino acid starvation. The starvation-induced enhancement of amino acid transport does not appear to be the result of a release from transinhibition. After 30 min of amino acid starvation, AIB transport is either unchanged or slightly decreased even though amino acid pools are already depleted. Furthermore, loading cells with high concentrations of a single amino acid following a period of amino acid starvation fails to prevent the enhancement of AIB transport, whereas incubation of the cells with the single amino acid for the entire duration of amino acid starvation prevents the enhancement; intracellular amino acid pools are similar under both conditions. The enhancement of amino acid transport requires concomitant RNA and protein synthesis, consistent with the view that the adaptive increase reflects an increased amount of a rate-limiting protein involved in the transport process. Dexamethasone, which dramatically inhibits AIB transport in cells incubated in amino acid-containing medium, both blocks the starvation-induced increase in AIB transport, and causes a time-dependent decrease in transport velocity in cells whose transport has previously been enhanced by starvation.

Amino Acids↗
PubMed1991

Starvation is associated with changes in the elemental composition of the pancreatic beta-cell.

By using the proton microprobe technique we have investigated the elemental composition of both pancreatic beta-cells and exocrine pancreas from fed and 24 h or 48 h starved obese hyperglycemic mice. Among the 15 elements measured in the beta-cells both Ca and Fe increased while Mg and S decreased significantly after 24 h of starvation, the effects being more pronounced after 48 h. When animals were starved for 48 h there was a decrease in the contents of Cl, Rb and Cu, whereas that of Al and Mn increased with 152 and 55%, respectively. There was an initial decrease in Na after 24 h of starvation, which was followed by an increase after 48 h. This is in contrast to Cd, which first increased and then decreased to a value lower than that obtained in the fed animal. The content of K showed a small decrease and that of Pb showed an increase only in the 24 h starved group. In the beta-cells the contents of Zn and P did not change subsequent to starvation. In the exocrine pancreas Na, Cl and P decreased after 24 h of starvation and except for Na, the decrease was maintained when the starvation period was increased to 48 h. After 24 h there was a significant, though transient, increase in K, Mg and Rb. With regard to the contents of Zn, Cu and S there was a progressive decrease as the starvation continued. In contrast to the endocrine pancreas the content of Al in the exocrine pancreas did not change after 48 h of starvation. There was no change in islet insulin content subsequent to starvation. The extent to which the observed changes in beta-cell elemental composition is involved in the impaired insulin release associated with starvation, merits further investigations.

Animals↗
PubMed1989

Small-intestinal function during enteral feeding and starvation in man.

1. Small-intestinal absorption and permeability were measured in nine patients with malnutrition who were receiving liquid enteral nutrition after different periods of starvation, in five patients receiving enteral nutrition without starvation, in six healthy subjects after starvation for 36 h and in two obese subjects starved for 11 days. 2. Absorption, expressed by the plasma 60 min D-xylose level and the plasma 60 min D-xylose/3-O-methyl-D-glucose ratio, was greatly decreased (P less than 0.001) in the nine patients receiving enteral feeding after starvation, whereas permeability, denoted by the 5 h urinary lactulose/rhamnose ratio, was increased (P less than 0.05). 3. The five patients receiving enteral feeds without prior starvation had normal intestinal absorption and permeability. 4. Starvation of the healthy subjects reduced absorption (P less than 0.05) and this was detectable at 36 h. Permeability, however, was not increased by 36 h starvation. Starvation of the obese subjects also progressively reduced absorption, and this was reversed with refeeding. 5. Changes in intestinal function during enteral feeding are similar to those seen in intestinal diseases. They develop rapidly and are not caused or reversed by liquid enteral feeds. Starvation, before beginning feeding, may explain some of the changes found.

Adult↗
PubMed1999

Body composition, resting and running metabolic rates, and net cost of running in rats during starvation.

Resting metabolic rate decreases during starvation. However, effects of starvation on the cost of running are not clear. The aim of this study was to examine the effects of 5 days starvation on body composition, resting metabolic rates, running metabolic rates, and net cost of running in male rats. Five days starvation resulted in reductions of 70% fat, 8% protein and 12% carbohydrates. Mass(-0.75) specific resting metabolic rate was significantly reduced from 3.69 +/- 0.27 to 2.73 +/- 0.17 W kg(-0.75) after 5 days starvation. The reduction in metabolic rate after 5 days starvation was maintained during running, in that running metabolic rate was reduced from 10.65 +/- 0.41 to 8.97 +/- 0.47 W kg(-0.75). The net costs of running were calculated and expressed as the costs of moving 1 kg a distance of 1 m. After 5 days of starvation it was reduced from 31.16 +/- 2.03-29.79 +/- 1.69 J m(-1) kg(-1). The reduction however was not significant. The present results therefore suggest that 5 days starvation resulted in a metabolic depression of the resting metabolic rate that was maintained during running. However, the net cost of running remained unchanged, suggesting that the muscle tissues are not significantly involved in the metabolic changes during starvation.

Animals↗
PubMed1987

Effects of starvation and refeeding on tissue zinc, copper and iron in turkey poults.

The effects of starvation and refeeding of 2-wk-old turkey poults on serum and tissue levels of zinc, copper and iron were investigated. Serum concentrations of zinc and copper declined during 4 d of starvation. Refeeding for 24 h following a period of starvation restored serum copper to levels similar to those in the fed controls but failed to elevate zinc levels. Liver concentrations and total quantities of zinc, copper and iron increased throughout starvation. Refeeding the starved poults reduced hepatic metal concentrations but caused a further increase in total metal content. This was apparently related to the large increase in liver mass, and the effect was most pronounced in poults starved 1 d prior to refeeding. Starvation also caused an increased zinc concentration and content and a reduced copper content in the pancreas, duodenal mucosa and kidney. Iron content of the pancreas and kidney increased during starvation, but that of the duodenal mucosa declined. Starvation evoked a progressive increase in the cytosolic zinc concentration from liver, pancreas, duodenal mucosa and kidney. A major part of this increase was accounted for as zinc bound to metallothionein (MT). Refeeding rapidly reduced cytosolic and MT-bound zinc in each of these tissues. It was concluded that starvation and refeeding had major effects on tissue trace metal status. A function is proposed for MT during starvation as a mechanism for the conservation of body zinc stores. Zinc, released as a consequence of tissue catabolism, is repartitioned into a soluble storage site (MT), which can be rapidly mobilized to meet the demands of new tissue synthesis once anabolic metabolism resumes.

Animal Nutritional Physiological Phenomena↗
PubMed1990

Diarrhoea of famine and malnutrition: investigations using a rat model. 1. Jejunal hypersecretion induced by starvation.

The effects of progressive starvation for up to three days on the secretory functions of the intestine were investigated using in vitro and in vivo preparations of rat jejunum and secretagogues whose action was either through cyclic AMP or Ca++. Initial starvation for 24 h (day 1) did not significantly alter the basal net electrogenic ion secretion measured in vitro as the short circuit current (Isc, muamps/cm2) or the change in electrogenic ion secretion (delta Isc) induced by the secretagogues. By day 2 of starvation, however, the maximum delta Isc transient induced by the cholinergic and other secretagogues (delta Isc = Isc max-basal Isc) was greatly increased (up to a maximum of 117%) compared with the fed controls on an area basis. The delta Isc were even greater on day 3 of starvation. If a tissue weight basis was used to normalise the data the increase became even more marked. The enhancement in secretion was not caused by a decrease in absorptive capacity as glucose, added mucosally, gave larger increases in absorptive currents in the starved than in the fed jejuna. Bethanecol dose-delta Isc response curves in fed and starved jejuna showed an increase in the maximum electrogenic secretion in the starved but no apparent change in the affinity of their cholinergic receptors mediating the enhanced secretion. The starvation-induced increase in secretion elicited by bethanecol was blocked by atropine, indicating that the receptors were muscarinic, but was unaffected by tetrodotoxin indicating that the enteric neural innervation was not essential for its expression. Noradrenaline released by tyramine was greater in the starved than the fed jejunum, suggesting that a decreased sympathetic tone was unlikely to be the major cause of the starvation induced secretory enhancement. Measurement of jejunal fluid movements in vivo showed that in fed controls and throughout the three days of starvation there was an unchanged net fluid absorption in the basal, unstimulated state. By day 2 and day 3 of starvation, however, bethanecol stimulated fluid secretion was very much greater than that of the fed controls. This increase in fluid secretion was concomitant with significant increases in the concentration of chloride in the lumenal fluid. Starvation thus appears to make the rat jejunum hypersensitive to cholinergic and other secretagogues, increasing the electrogenic secretion of chloride in vitro and that of chloride and fluid in vivo. These results obtained with the rat model give a new insight into possible mechanisms by which the diarrhoea of human famine and malnutrition may be expressed.

Animals↗
PubMed1997

Glucoregulation during progressive starvation in late pregnancy in the rat.

The response of glucose utilization (transport and phosphorylation) by individual skeletal muscles to progressive starvation in late pregnancy in the rat was investigated in relation to changes in whole body glucose turnover. Compared with insulin-stimulated values, the decline in muscle glucose utilization evoked by short-term (6-h) starvation was about twofold greater in pregnancy. Suppression of glucose utilization by slow-twitch muscles was observed as the starvation period was extended from 6 to 24 h only in unmated rats. Extending starvation to 24 h did not further reduce glucose utilization by fast-twitch skeletal muscles in either group. Suppression of whole body glucose disposal was observed between 6 and 24 h of starvation in unmated, but not pregnant, rats. The results demonstrate that metabolic adaptation of almost complete suppression of glucose utilization by slow-twitch muscle, normally elicited only by prolonged (24-h) starvation, is already established after acute (6-h) starvation in late pregnancy. The present study supports the concept of "accelerated starvation" in late pregnancy with respect to muscle glucose utilization after short-term food withdrawal but demonstrates that further glucose conservation cannot be achieved after more prolonged starvation.

Animals↗
PubMed1983

Starvation and hypothyroidism exert an overlapping influence on rat hepatic messenger RNA activity profiles.

To assess the effect of starvation and to explore the potential interrelationship of starvation and thyroid status at the pretranslational level, we have analyzed by two-dimensional gel electrophoresis, the hepatic translational products of starved and fed euthyroid and hypothyroid rats. 5 d of starvation resulted in a statistically significant change in 27 of 240 products visualized, whereas hypothyroidism caused a change in 20, both in comparison with the fed euthyroid state. Of considerable interest was that 68% of all changing messenger (m)RNA sequences were common to the hypothyroid and starved groups and showed the same directional shift. Further, both starvation and hypothyroidism yielded comparable decreases in total hepatic cytoplasmic RNA content. Although it has been well established that the level of circulating triiodothyronine (T3) and the level of hepatic nuclear receptors fall in starvation, this reduction cannot account for the observed decrease of total hepatic RNA nor for all of the alterations in the concentrations of specific mRNA sequences. Thus, administration of T3 to starved animals in a dose designed to occupy all nuclear T3 receptors fails to prevent the fall in total RNA and the majority of starvation-induced changes in the level of mRNA sequences. Moreover, starvation of athyreotic animals results in a further decrease in total RNA and in a further change in the level of individual mRNA species. We conclude, therefore, that although the reduced levels of circulating T3 and the nuclear T3 receptors can contribute to the observed results of starvation, the starvation-induced changes are not exclusively mediated by this factor. The striking overlap in the genomic response between hypothyroid and starved animals raises the possibility that those biochemical mechanisms regulated at a pretranslational level by T3 are either not helpful or injurious to the starving animal. The reduction in circulating T3 and nuclear receptor sites together with T3-independent mechanisms initiated in the starved animal may constitute redundant processes designed to conserve energy and substrate in the nutritionally deprived organism.

Animals↗
PubMed2000

Fibre-type specific modification of the activity and regulation of skeletal muscle pyruvate dehydrogenase kinase (PDK) by prolonged starvation and refeeding is associated with targeted regulation of PDK isoenzyme 4 expression.

Using immunoblot analysis with antibodies raised against recombinant pyruvate dehydrogenase kinase (PDK) isoenzymes PDK2 and PDK4, we demonstrate selective changes in PDK isoenzyme expression in slow-twitch versus fast-twitch skeletal muscle types in response to prolonged (48 h) starvation and refeeding after starvation. Starvation increased PDK activity in both slow-twitch (soleus) and fast-twitch (anterior tibialis) skeletal muscle and was associated with loss of sensitivity of PDK to inhibition by pyruvate, with a greater effect in anterior tibialis. Starvation significantly increased PDK4 protein expression in both soleus and anterior tibialis, with a greater response in anterior tibialis. Starvation did not effect PDK2 protein expression in soleus, but modestly increased PDK2 expression in anterior tibialis. Refeeding for 4 h partially reversed the effect of 48-h starvation on PDK activity and PDK4 expression in both soleus and anterior tibialis, but the response was more marked in soleus than in anterior tibialis. Pyruvate sensitivity of PDK activity was also partially restored by refeeding, again with the greater response in soleus. It is concluded that targeted regulation of PDK4 isoenzyme expression in skeletal muscle in response to starvation and refeeding underlies the modulation of the regulatory characteristics of PDK in vivo. We propose that switching from a pyruvate-sensitive to a pyruvate-insensitive PDK isoenzyme in starvation (a) maintains a sufficiently high pyruvate concentration to ensure that the glucose-->alanine-->glucose cycle is not impaired, and (b) may 'spare' pyruvate for anaplerotic entry into the tricarboxylic acid cycle to support the entry of acetyl-CoA derived from fatty acid (FA) oxidation into the tricarboxylic acid cycle. We further speculate that FA oxidation by skeletal muscle is both forced and facilitated by upregulation of PDK4, which is perceived as an essential component of the operation of the glucose-FA cycle in starvation.

Animals↗
PubMed1993

How do non-differentiating bacteria adapt to starvation?

Non-differentiating bacteria adapt to starvation induced growth arrest by a complex turn-on/turn-off pattern of protein synthesis. This response shows distinct similarities with those of spore formation in differentiating organisms. A substantial amount of information on the non-growth biology of non-differentiating bacteria can be derived from studies on Vibrio strains. One important result is that carbon rather than nitrogen or phosphorus starvation leads to the development of a starvation and stress resistant cell in these organisms. Hence, we have attempted to characterize the carbon starvation stimulon. By the use of two-dimensional gel electrophoresis of pulse-labelled cells and transposon mutagenesis, using reporter gene constructs, the identity and function of some members of the carbon starvation stimulon have been elucidated. Moreover, regulatory genes of the starvation response have been identified with these techniques. Current studies primarily address the identity and function of these genes. The role of transcript modification and stability for both long term persistence during starvation as well as the efficient recovery of cells which occurs upon nutrient addition is also addressed. It is suggested that an understanding of the functionality of the translational machinery is essential for the understanding of these adaptive pathways. This contribution also discusses the diversity of the differentiation-like response to starvation in different bacteria and whether a general starvation induced programme exists.

Adaptation, Physiological↗
PubMed2002

Physiological role of the GlnK signal transduction protein of Escherichia coli: survival of nitrogen starvation.

Escherichia coli contains two PII-like signal trans-duction proteins, PII and GlnK, involved in nitrogen assimilation. We examined the roles of PII and GlnK in controlling expression of glnALG, glnK and nac during the transition from growth on ammonia to nitrogen starvation and vice versa. The PII protein exclusively controlled glnALG expression in cells adapted to growth on ammonia, but was unable to limit nac and glnK expression under conditions of nitrogen starvation. Conversely, GlnK was unable to limit glnALG expression in cells adapted to growth on ammonia, but was required to limit expression of the glnK and nac promoters during nitrogen starvation. In the absence of GlnK, very high expression of the glnK and nac promoters occurred in nitrogen-starved cells, and the cells did not reduce glnK and nac expression when given ammonia. Thus, one specific role of GlnK is to regulate the expression of Ntr genes during nitrogen starvation. GlnK also had a dramatic effect on the ability of cells to survive nitrogen starvation and resume rapid growth when fed ammonia. After being nitrogen starved for as little as 10 h, cells lacking GlnK were unable to resume rapid growth when given ammonia. In contrast, wild-type cells that were starved immediately resumed rapid growth when fed ammonia. Cells lacking GlnK also showed faster loss of viability during extended nitrogen starvation relative to wild-type cells. This complex phenotype resulted partly from the requirement for GlnK to regulate nac expression; deletion of nac restored wild-type growth rates after ammonia starvation and refeeding to cells lacking GlnK, but did not improve viability during nitrogen starvation. The specific roles of GlnK during nitrogen starvation were not the result of a distinct function of the protein, as expression of PII from the glnK promoter in cells lacking GlnK restored the wild-type phenotypes.

Ammonia↗
PubMed1992

Variations in rRNA content of marine Vibrio spp. during starvation-survival and recovery.

The degree and temporal context of variations in ribosome content during nutrient starvation of two copiotrophic marine bacteria, Vibrio alginolyticus and Vibrio furnissii, have been examined. The organisms were starved either by nutritional shift-down or by consumption of limiting nutrients resulting from growth into stationary phase. Measurements of the amount of hybridization to 16S rRNA-specific probes revealed that the cells retained between 10 and 26% of their original rRNA content after 15 days of starvation. In V. alginolyticus, losses in stationary-phase cells occurred rapidly (1 to 2 days), whereas cells shifted into starvation remained larger and retained considerably more rRNA. The ability of V. alginolyticus to recover from starvation was assessed after cells were maintained for 2, 8, and 15 days in nutrient-depleted medium. The pattern of recovery at the level of rRNA accumulation depended upon the duration of nutrient deprivation and the manner in which it was imposed. Stationary-phase cells starved for 2 days had only slight relative increases in rRNA levels after excess nutrients were added. As the duration of starvation lengthened to 8 and 15 days, increasingly greater amounts of rRNA (30 and 70 times preenrichment values, respectively) were transcribed after nutrient enrichment. Shift-down cells recovered from 2 and 8 days of starvation without extensive rRNA production. After 15 days, nutrient enrichment caused 16S rRNA levels to increase 30-fold. The results indicate that the mechanisms controlling starvation-survival in these marine bacterial species are linked to the physiological state at the onset of starvation and that the subsequent pattern of recovery will depend upon how starvation was initiated.

Kinetics↗