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

Four starvation-inducible loci (stiA, stiB, stiC, and stiE) of Salmonella typhimurium have been extensively characterized as to their genetic and physiologic regulation, and their roles in survival during prolonged simultaneous phosphate (P)-, carbon (C)- and nitrogen (N)-starvation (PCN-starvation). Strains of S. typhimurium LT-2, isogenic with the exception of lacking either the stiA, stiB or stiC locus, died off more quickly and survived at much reduced levels compared with their wild-type parent. When certain sti mutations were combined in the same strain, we found that viability of these cultures declined even more rapidly, and starvation-survival was affected to levels over-and-above the additive effects of each individual mutation, indicating an epistatic relationship between these loci. All four sti loci were, directly or indirectly, under negative control by the crp gene product (cAMP receptor protein, CRP). With the exception of stiB, all were similarly regulated by the cya gene product (i.e., cAMP). This suggests that CRP acts alone, or with a signal molecule other than cAMP, to cause repression of the stiB locus. In addition, all four loci are under positive regulation by the relA gene product (i.e., ppGpp) during C- or N-starvation, but not P-starvation. Since not all relA-dependent sti loci are induced during both C- and N-starvation, we propose that two separate ppGpp-dependent pathways function during C-starvation and N-starvation, respectively. Possible models for separate P-, C- and N-starvation-induction pathways are discussed.
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PMID:Starvation-inducible loci of Salmonella typhimurium: regulation and roles in starvation-survival. 132 Jul 26

The gene products of the ugp operon of Escherichia coli are responsible for the uptake of sn-glycerol-3-phosphate and certain glycerophosphodiesters. The regulation of ugp is mainly phoBR-dependent. Significant expression, however, can be observed even in the presence of high concentrations of phosphate, a condition which normally completely represses pho expression. Pho-independent ugp expression was found to be derepressed during the late logarithmic growth phase due to carbon starvation. Among different carbon sources tested, glucose caused the most complete repression. Addition of cAMP prevented glucose repression, indicating that a cAMP-CRP control mechanism may be directly or indirectly involved in the carbon-starvation response. This conclusion is supported by the fact that pho-independent ugp expression correlated with the presence of the cya and crp gene products.
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PMID:Carbon-starvation induction of the ugp operon, encoding the binding protein-dependent sn-glycerol-3-phosphate transport system in Escherichia coli. 174 36

The ugp operon of Escherichia coli includes genes involved in the uptake of sn-glycerol-3-phosphate and glycerophosphoryl diesters and belongs to the pho regulon which is induced by phosphate limitation. This operon has two transcriptional initiation sites, as determined by S1 nuclease mapping of the in vivo transcripts. The downstream promoter has multiple copies of the pho box, the consensus sequence shared by the pho promoters; the upstream promoter has a consensus sequence for the promoters regulated by cyclic AMP and its receptor protein, CRP. PhoB protein, which is the transcriptional activator for the pho regulon, protected the regulatory region with the pho boxes in DNase I footprinting experiments and activated transcription from the downstream promoter in vitro. Studies with transcriptional fusions between ugp and a promoterless gene for chloramphenicol acetyltransferase show that the upstream promoter is induced by carbon starvation in a manner that required the cya and crp genes. PhoB protein may act as a repressor for this upstream promoter, which also overlaps the upstream third pho box. The downstream promoter was induced by phosphate starvation and requires the PhoB protein for its activation as do the other pho regulon promoters. These results suggest that the two promoters function alternately in responding to phosphate or carbon starvation, thus providing the cell with a means to adapt to these physiological stresses.
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PMID:Dual regulation of the ugp operon by phosphate and carbon starvation at two interspaced promoters. 198 50

Luminescence in the marine bacterium, Vibrio fischeri, is regulated by a small molecule, the autoinducer. The transcription of the V. fischeri lux genes also requires a regulatory protein, (luxR), cAMP and CRP. We show that, apart from these components, the transcription of the PR lux operon is also controlled by the activity of sigma 32 (htpR protein). In luminescent Escherichia coli (E. coli/pChv1), as well as in different marine luminous bacteria and their naturally occurring dark (K) variants, the luminescence system can be induced by starvation under microaerophilic conditions. Heat shock also induces luminescence in htpR+ but not in htpR- strains of E. coli/pChv1. An htpR- mutant of E. coli containing pChv1 is very dim and its luminescence is not induced by starvation or heat shock. The addition of a plasmid bearing the gene for htpR+ into such cells restores their response to starvation and heat shock. Cells of wild type E. coli/pChv1 that have been starved or heat shocked respond to lower concentrations of V. fischeri inducer than untreated cells. These cultures also produce more extracellular inducer than untreated cells. Starvation, heat shock and the presence of sigma 32 do not induce luminescence in luxl deleted E. coli/pChv1 cells. SOS-inducing agents advance the onset of luminescence in both htpR+ and htpR- strains but not in luxl deleted E. coli/pChvi cells. DNA sequencing of the luxR-luxl region reveals the presence of a promoter region of the kind typical for sigma 32 at the beginning of the luxl gene. In addition we find a LexA protein-DNA binding site in the non-consensus sequence for the -35 region of the PR operon. It is proposed that the regulatory protein-inducer complex displaces the LexA protein and allows the transcription of the right operon. SOS-inducing agents result in proteolysis of LexA protein and advance the onset of luminescence. sigma 32 enhances the transcription from the PR operon and thus initiates a positive control circuit. It seems that sigma 32 is the major controlling element in determining the onset of luminescence both in vivo and in vitro.
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PMID:The transcription of bacterial luminescence is regulated by sigma 32. 306 68

The second vegetative sigma factor sigma S (encoded by the rpoS gene) is the master regulator in a complex regulatory network that governs the expression of many stationary phase-induced and osmotically regulated genes in Escherichia coli. Using a combination of gene-fusion technology and quantitative immunoblot, pulse-labeling, and immunoprecipitation analyses, we demonstrate here that rpoS/sigma S expression is not only transcriptionally controlled, but is also extensively regulated at the levels of translation and protein stability. rpoS transcription is inversely correlated with growth rate and is negatively controlled by cAMP-CRP. In complex medium rpoS transcription is stimulated during entry into stationary phase, whereas in minimal media, it is not significantly induced. rpoS translation is stimulated during transition into stationary phase as well as by an increase in medium osmolarity. A model involving mRNA secondary structure is suggested for this novel type of post-transcriptional growth phase-dependent and osmotic regulation. Furthermore, sigma S is a highly unstable protein in exponentially growing cells (with a half-life of 1.4 min), that is stabilized at the onset of starvation. When cells are grown in minimal glucose medium, translational induction and sigma S stabilization occur in a temporal order with the former being stimulated already in late exponential phase and the latter taking place at the onset of starvation. Although sigma S does not control its own transcription, it is apparently indirectly involved in a negative feedback control that operates on the post-transcriptional level. Our analysis also indicates that at least five different signals [cAMP, a growth rate-related signal (ppGpp?), a cell density signal, an osmotic signal, and a starvation signal] are involved in the control of all these processes that regulate rpoS/sigma S expression.
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PMID:The cellular concentration of the sigma S subunit of RNA polymerase in Escherichia coli is controlled at the levels of transcription, translation, and protein stability. 752 5

During transition into stationary phase a large set of proteins is induced in Escherichia coli. Only a minority of the corresponding genes has been identified so far. Using the lambda placMu system and a plate screen for carbon starvation-induced fusion activity, a series of chromosomal lacZ fusions (csi::lacZ) was isolated. In complex medium these fusions were induced either during late exponential phase or during entry into stationary phase. csi::lacZ expression in minimal media in response to starvation for carbon, nitrogen and phosphate sources and the roles of global regulators such as the alternative sigma factor sigma s (encoded by rpoS), cAMP/CRP and the relA gene product were investigated. The results show that almost every fusion exhibits its own characteristic pattern of expression, suggesting a complex control of stationary phase-inducible genes that involves various combinations of regulatory mechanisms for different genes. All fusions were mapped to the E. coli chromosome. Using fine mapping by Southern hybridization, cloning, sequencing and/or phenotypic analysis, csi-5, csi-17, and csi-18 could be localized in osmY (encoding a periplasmic protein), glpD (aerobic glycerol-3-phosphate dehydrogenase) and glgA (glycogen synthase), respectively. The other fusions seem to specify novel genes now designated csiA through to csiF. csi-17(glpD)::lacZ was shown to produce its own glucose-starvation induction, thus illustrating the intricacies of gene-fusion technology when applied to the study of gene regulation.
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PMID:Identification and characterization of stationary phase-inducible genes in Escherichia coli. 793 31

The main determinant of the plant pathogen Erwinia chrysanthemi virulence is the production of extracellular enzymes, mainly pectate lyases. Adjacent to a pectate lyase encoding locus, we identified the gene rotA supposed to encode a folding catalyst. Overproduction of the protein and assay of activity using a synthetic substrate, confirmed that rotA encodes a periplasmic peptidyl-prolyl cis-trans isomerase. rotA disruption provokes no change in cell morphology, cell viability, growth rate or stability of the extracellular and periplasmic proteins. In addition, this mutation does not alter the activity of the pectate lyases, their stability in the periplasm during the transitory step of secretion or their recognition by the Out secretory system. rotA expression was followed using a rotA::uidA transcriptional fusion. Some environmental conditions, such as temperature variations and nitrogen starvation, modulate rotA expression. In contrast to the E. coli rotA gene, the E. chrysanthemi rotA possesses only one promoter and is not controlled by the CRP global regulator.
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PMID:Characterization of a periplasmic peptidyl-prolyl cis-trans isomerase in Erwinia chrysanthemi. 941 40

The general stress-induced sigma subunit sigma s of Escherichia coli RNA polymerase is closely related to the vegetative sigma factor sigma 70. In view of their very similar promoter specificity in vitro, it is unclear how sigma factor selectivity in the expression of sigma s-dependent genes is generated in vivo. The csiD gene is such a strongly sigma s-dependent gene. In contrast to sigma s, which is induced in response to many different stresses, csiD, whose expression is driven from a single promoter, is induced by carbon starvation only. To our knowledge, the csiD promoter is the first characterized promoter which is not only exclusively dependent on sigma s-containing RNA polymerase (E sigma s), but also requires an activator, cAMP-CRP. In addition, leucine-responsive regulatory protein (Lrp) acts as a positive modulator of csiD expression. Also in vitro, E sigma s is more efficient than E sigma 70 in csiD promoter binding, open complex formation and run-off transcription, which might be due to the poor match of the csiD -35 region to the sigma 70 consensus and to transcription by E sigma s being less dependent on contacts in this region. By DNase I protection experiments, a cAMP-CRP binding site centered at -68.5 nucleotides upstream of the csiD transcriptional start site was identified. While cAMP-CRP stimulates E sigma 70 binding, it does not promote open complex formation by E sigma 70, but does so in conjunction with E sigma s. With linear templates, cAMP-CRP significantly stimulates E sigma s-mediated in vitro transcription, whereas transcription by E sigma 70 is negligible and hardly stimulated by cAMP-CRP. These findings may reflect different or less stringent positional requirements for an activator site for E sigma s than for E sigma 70, and indicate that cAMP-CRP contributes to sigma factor selectivity at the csiD promoter. In vitro transcription experiments with super-coiled templates, however, revealed significant cAMP-CRP-stimulated transcription also by E sigma 70. Yet, under these conditions, H-NS was found to restore E sigma s specificity by strongly interfering with cAMP-CRP/E sigma 70-dependent transcription. Lrp strongly and cooperatively binds to multiple sites located between positions -14 and -102 (in a way that suggests DNA wrapping around multiple Lrp molecules) and moderately stimulates in vitro transcription, especially with E sigma s. In summary, we conclude that the csiD promoter has an intrinsic preference for E sigma s, but that also protein factors such as cAMP-CRP, Lrp and probably H-NS as well as DNA conformation contribute to its strong E sigma s selectivity. Furthermore, this strong E sigma s preference in combination with a requirement for high concentrations of the essential activator cAMP-CRP ensures csiD expression under conditions of carbon starvation, but not other stress conditions.
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PMID:Molecular analysis of the regulation of csiD, a carbon starvation-inducible gene in Escherichia coli that is exclusively dependent on sigma s and requires activation by cAMP-CRP. 951 7

Salmonella serovars are common etiologic agents of intestinal-based disease of animals and humans. As a result of their lifestyle, salmonellae occupy and survive in a wide range of niches where they can encounter an even broader range of environmental stresses. One of the most common stresses is starvation for an essential nutrient such as a carbon/energy (C)-source. The genetic and physiologic changes that the bacterium undergoes in response to starvation-stress are referred to as the starvation-stress response or SSR. The genetic loci whose expression increases in response to the starvation-stress compose the SSR stimulon. Several loci of the SSR stimulon have been identified in Salmonella typhimurium and grouped, based on putative or known functions or products, into transport systems, C-compound catabolic enzymes, known protective enzymes, respiratory enzyme systems, regulatory proteins, virulence loci and unclassified products. The majority of loci identified are under positive control by the rpoS-encoded sigma factor, sigma S. However, a few are under (indirect) negative control by sigma S, but only during starvation-induced stationary phase. Most of the loci identified are also under either positive or negative control by the cAMP:CRP complex. For many, additional regulatory proteins (e.g. FadR, OxyR, and RelA and others) play a role in their regulation as well. Furthermore, most of the SSR loci identified are induced during other stresses or environmental conditions. For example, some are induced during P- or N-starvation, in addition to C-starvation; some are induced by extremes in pH or osmolarity; and some are induced in the intracellular environment of epithelial cells, and/or macrophages, and/or medium designed to mimic the intracellular milieu of mammalian cells (ISM). Several SSR loci are required for long-term starvation-survival (core SSR loci), e.g. narZ, dadA, stiC and rpoS. In addition, a few of the core SSR loci are also required for stress-specific-inducible and/or C-starvation-inducible resistance to H2O2 (e.g. stiC), thermal (e.g. stiC), and/or acid pH (e.g. narZ), challenge. Interestingly, C-starved cells are resistant to challenge with the antimicrobial peptide, polymyxin B. However, this resistance mechanism(s) is different from the resistance mechanisms for H2O2 and other environmental stresses. Furthermore, a link between the SSR and Salmonella virulence can be hypothesized since the two major regulators of the SSR, sigma s and cAMP:CRP, are required for full virulence of Salmonella. Moreover, the spv (Salmonella plasmid-associated virulence) genes, required for Salmonella to cause systemic disease, are C (and P- and N-)-starvation-inducible. However, a direct link between starvation-stress and virulence has not been established conclusively.
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PMID:The starvation-stress response (SSR) of Salmonella. 988 80

Erwinia chrysanthemi 3937 secretes an arsenal of pectinolytic enzymes including several pectate lyases encoded by the pel genes. We characterized a novel cluster of pectinolytic genes consisting of the three adjacent genes pehV, pehW and pehX, whose products have polygalacturonase activity. The high similarity between the three genes suggests that they result from duplication of an ancestral gene. The transcription of pehV, pehW and pehX is dependent on several environmental conditions. They are induced by pectin catabolic products and this induction results from inactivation of the KdgR repressor which controls almost all the steps of pectin catabolism. The presence of calcium ions strongly reduced the transcription of the three peh genes. Their expression was also affected by growth phase, osmolarity, oxygen limitation and nitrogen starvation. In addition, the pehX transcription is affected by catabolite repression and controlled by the activator protein CRP. PecS, which was initially isolated as a repressor of virulence factors, acts as an activator of the peh transcription. We showed that the three regulators KdgR, PecS and CRP act by direct interaction with the promoter regions of the peh genes. Analysis of simultaneous binding of KdgR, PecS, CRP and RNA polymerase indicated that the activator effect of PecS results from a competition between PecS and KdgR for the occupation of overlapping binding sites. Thus, to activate peh transcription, PecS behaves as an anti-repressor against KdgR.
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PMID:Analysis of three clustered polygalacturonase genes in Erwinia chrysanthemi 3937 revealed an anti-repressor function for the PecS regulator. 1056 5


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