Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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

When deprived of essential nutrients, the non-diazotrophic cyanobacterium Synechococcus sp. strain PCC 7942 undergoes a proteolytic degradation of the phycobiliproteins, its major light-harvesting pigments. This process is known as chlorosis. This paper presents evidence that the degradation of phycobiliproteins is part of an acclimation process in which growing cells differentiate into non-pigmented cells able to endure long periods of starvation. The time course of degradation processes differs for various photosynthetic pigments, for photosystem I and photosystem II activities and is strongly influenced by the illumination and by the experimental conditions of nutrient deprivation. Under standard experimental conditions of combined nitrogen deprivation, three phases of the differentiation process can be defined. The first phase corresponds to the well-known phycobiliprotein degradation, in phase 2 the cells lose chlorophyll a prior to entering phase 3, the fully differentiated state, in which the cells are still able to regenerate pigmentation after the addition of nitrate to the culture. An analysis of the protein synthesis patterns by two-dimensional gel electrophoresis during nitrogen starvation indicates extensive differential gene expression, suggesting the operation of tight regulatory mechanisms.
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PMID:Nitrogen-starvation-induced chlorosis in Synechococcus PCC 7942: adaptation to long-term survival. 978 92

Pseudanabaena sp. strain PCC 6903 is the first cyanobacteria lacking the typical prokaryotic glutamine synthetase type I encoded by the glnA gene. The glnN gene product, glutamine synthetase type III, is the only glutamine synthetase activity present in this cyanobacterium. Analysis of glnN expression clearly indicated a nitrogen-dependent regulation. Pseudanabaena glnN gene expression and GSIII activity were upregulated under nitrogen starvation or using nitrate as a nitrogen source, while low levels of transcript and activity were found in ammonium-containing medium. Primer extension analysis showed that the glnN gene promoter structure resembled that of the NtcA-related promoters. Mobility shift assays demonstrated that Synechocystis sp. PCC 6803 NtcA protein, expressed and purified from Escherichia coli, bound to the promoter of the Pseudanabaena 6903 glnN gene. The NtcA control of the glnN gene in this cyanobacterium suggested that, in the absence of a glnA gene, NtcA took control of the only glutamine synthetase gene in a fashion similar to the way the glnA gene is governed in those cyanobacteria harbouring a glnA gene.
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PMID:Nitrogen control of the glnN gene that codes for GS type III, the only glutamine synthetase in the cyanobacterium Pseudanabaena sp. PCC 6903. 998 84

Constitutively activated mutants of the Ras-related protein TC21/R-Ras2 cause tumorigenic transformation of NIH3T3 cells. However, unlike Ras, TC21 fails to bind to and activate the Raf-1 serine-threonine kinase. Thus, whereas Ras transformation is critically dependent on Raf-1 TC21 activity is promoted by activation of Raf-independent signaling pathways. In the present study, we have further compared the functions of Ras and TC21. First we determined the basis for the inability of TC21 to activate Raf-1. Whereas Ras can interact with the two distinct Ras-binding sequences in NH2-terminus of Raf-1, designated RBS1 and Raf-Cys, TC21 could only bind Raf-Cys. Thus, the inability of TC21 to bind to RBS1 may prevent it from promoting the translocation of Raf-1 to the plasma membrane. Second, we found that TC21 is an activator of the JNK and p38, but not ERK, mitogen-activated protein kinase cascades and that TC21 transforming activity was dependent on Rac function. Thus, like Ras, TC21 may activate a Rac/JNK pathway. Third, we determined if TC21 could cause the same biological consequences as Ras in three distinct cell types. Like Ras, activated TC21 caused transformation of RIE-1 rat intestinal epithelial cells and terminal differentiation of PC12 pheochromocytoma cells. Finally, activated TC21 blocked serum starvation-induced differentiation of C2 myoblasts, whereas dominant negative TC21 greatly accelerated this differentiation process. Therefore, TC21 and Ras share indistinguishable biological activities in all cell types that we have evaluated. These results support the importance of Raf-independent pathways in mediating the actions of Ras and TC21.
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PMID:TC21 and Ras share indistinguishable transforming and differentiating activities. 1032 35

Adrenomedullin is a novel vasodilatory peptide originally isolated from pheochromocytoma. Recently, we found that adrenomedullin acts as an autocrine/paracrine apoptosis survival factor for rat endothelial cells. In the present study, we show that adrenomedullin induces the expression of Max, a heterodimeric partner of c-Myc, which may contribute to its ability to rescue endothelial cells from apoptosis. Max is a basic-helix-loop-helix-leucine zipper protein that forms heterodimers with its alternative partners, Mad and Mxi-1, to behave as an antagonist for Myc-Max heterodimer through competition for common DNA targets. The expression of Max is reported to be constitutive and more stable than c-Myc, and serum induces immediate c-Myc stimulation followed by modest Max up-regulation. In quiescent rat endothelial cells, adrenomedullin stimulated the expression of Max without affecting c-Myc. Quantitation with real-time quantitative PCR detected on the ABI Prism 7700 Sequence Detection System revealed that adrenomedullin and calcitonin gene-related peptide (CGRP), as well as serum, up-regulated Max mRNA levels and that down-regulation of Max mRNA after serum deprivation was prevented by adrenomedullin. Neither adrenomedullin nor CGRP affected c-Myc expression. Transfection of a Max-expressing plasmid into endothelial cells rescued the apoptosis induced by serum deprivation. Neutralization with anti-adrenomedullin antiserum or blockade with a CGRP receptor antagonist, CGRP(8-37), reduced Max mRNA levels in growing endothelial cells and enhanced apoptosis after serum starvation. Introduction of an antisense oligodeoxynucleotide against Max mRNA using transferrin receptor-operated transfer led to inhibition of both adrenomedullin-induced up-regulation of Max transcripts and its cell survival effect, whereas random, sense, or missense oligonucleotides were without effect. The negative regulation of E-box-driven transcription by adrenomedullin was demonstrated by using preproendothelin-1 promoter containing c-Myc-Max binding consensus sequence; the promoter activity of preproendothelin-1 was reduced by cotransfecting Max- and Mad-expressing plasmids as well as addition of adrenomedullin and CGRP. The present results demonstrate that adrenomedullin antagonizes serum deprivation-induced endothelial apoptosis by up-regulation of the max gene in an autocrine/ paracrine manner.
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PMID:Induction of max by adrenomedullin and calcitonin gene-related peptide antagonizes endothelial apoptosis. 1044 8

Freshwater species of the cyanobacterial genus Synechococcus import NaCl passively, and export Na(+) actively, by means of primary and secondary extrusion mechanisms. As a result of the ion and water fluxes, cell volumes are enlarged. We show in this paper that the NaCl-induced volume enlargement of Synechococcus sp. PCC 7942 cells is attended by a rapid (k = 0.39 s(-1)) increase in chlorophyll (Chl) a fluorescence. The cell turgor threshold (measured by osmotic titration of Chl a fluorescence) was lower in the absence of NaCl (0.195 Osm kg(-1)) than in the presence of 0.4 M NaCl (0.248 Osm kg(-1)) indicating NaCl uptake by the cells. Turgor thresholds of cells suspended in NaCl-containing medium were enlarged further by protonophoric uncouplers, P-type ATPase inhibitors, and light starvation, conditions that are known to interfere with the active extrusion of Na(+) ions. Cell swelling exerts probably a regulation on the distribution of phycobilisome (PBS) excitation between photosystem II (fluorescent Chl a) and photosystem I (nonfluorescent Chl a), since it affects PBS-sensitized Chl a fluorescence, but not directly excited Chl a fluorescence. The dependence of the Chl a fluorescence of cyanobacteria on cell volumes allows probing of bioenergetic phenomena that are related to dynamic osmotic volume changes, transmembrane solute and water fluxes, plasma membrane permeabilities, and internal osmotic conditions of cyanobacterial cells. Thus, cyanobacteria may serve as quite convenient models of aquatic microorganisms in experimental studies directed toward the elucidation of perception mechanisms and defense mechanisms of water and solute stresses.
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PMID:Sodium chloride-induced volume changes of freshwater cyanobacterium Synechococcus sp. PCC 7942 cells can be probed by chlorophyll a fluorescence. 1051 Feb 83

The nondiazotrophic cyanobacterium Synechococcus sp. strain PCC 7942 responds to nitrogen deprivation by differentiating into nonpigmented resting cells able to survive prolonged periods of starvation. The degradation of photosynthetic pigments, termed chlorosis, proceeds in an ordered manner in which the light-harvesting phycobiliproteins are degraded prior to chlorophyll. Here, we show that the function of the global transcription activator of nitrogen-regulated genes, NtcA, is required for the sequential pigment degradation and cell survival. The P(II) protein, known to signal the nitrogen status of the cells, is most probably not involved in the perception of the nitrogen-starvation-specific signal since in a mutant lacking P(II), chlorosis proceeded in the same manner as in the wild type. Inhibition of glutamine synthetase with l-methionine sulfoximine led to a rapid decrease of apc mRNA and to an increase of nblA mRNA levels, which is characteristic for nitrogen deprivation, suggesting that nitrogen starvation is sensed by a metabolic signal connected to glutamine synthetase activity. However, l-methionine sulfoximine treatment did not induce phycobiliprotein degradation, but led to an immediate cessation of this proteolytic process after its induction by nitrogen deprivation. This suggests that the proteolytic activity elicited by the expression of nblA has to be supported by glutamine synthetase activity.
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PMID:Nitrogen starvation in synechococcus PCC 7942: involvement of glutamine synthetase and NtcA in phycobiliprotein degradation and survival 1052 42

Synechocystis sp. PCC 6803 glutamine synthetase type I (GS) activity is controlled by direct interaction with two inactivating factors (IF7 and IF17). IF7 and IF17 are homologous polypeptides encoded by the gifA and gifB genes respectively. We investigated the transcriptional regulation of these genes. Expression of both genes is maximum in the presence of ammonium, when GS is inactivated. Nitrogen starvation attenuates the ammonium-mediated induction of gifA and gifB as well as the ammonium-mediated inactivation of GS. Putative binding sites for the transcription factor NtcA were identified at -7.5 and -30.5 bp upstream of gifB and gifA transcription start points respectively. Synechocystis NtcA protein binding to both promoters was demonstrated by gel electrophoresis mobility shift assays. Constitutive high expression levels of both genes were found in a Synechocystis NtcA non-segregated mutant (SNC1), which showed a fourfold reduction in the ntcA expression. These experiments indicate a repressive role for NtcA on the transcription of gifA and gifB genes. Our results demonstrate that NtcA plays a central role in GS regulation in cyanobacteria, stimulating transcription of the glnA gene (GS structural gene) and suppressing transcription of the GS inactivating factor genes gifA and gifB.
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PMID:NtcA represses transcription of gifA and gifB, genes that encode inhibitors of glutamine synthetase type I from Synechocystis sp. PCC 6803. 1071 99

Apoptosis in neuronal tissue is an efficient mechanism which contributes to both normal cell development and pathological cell death. The present study explored the effects of extracellular ATP on starvation-induced apoptosis in rat pheochromocytoma PC12 cells. Incubation of differentiated PC12 cells with ATP for 6h suppressed apoptosis. 2-Methylthio-ATP, a P2 purinoceptor agonist, was as potent as ATP in suppressing apoptosis, whereas adenosine, ADP, alpha,betamethylene-ATP or UTP was totally ineffective. The suppressive action of ATP was dependent upon the presence of extracellular Ca2+ and blocked by co-incubation with the P2 antagonist, suramin. DNA ladder formation, a typical symptom of apoptosis in starved cells, was inhibited by ATP, 2-methylthio-ATP but not by UTP. These results suggest that the inhibitory action of extracellular ATP on apoptotic cell death is mediated via the activation of P2X2 receptors in differentiated PC12 cells.
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PMID:Extracellular ATP inhibits starvation-induced apoptosis via P2X2 receptors in differentiated rat pheochromocytoma PC12 cells. 1080 82

The devH gene was identified in a screen for Anabaena sp. strain PCC 7120 sequences whose transcripts increase in abundance during a heterocyst development time course. The product of devH contains a helix-turn-helix motif similar to the DNA binding domain of members of the cyclic AMP receptor protein family, and the protein is most closely related to the cyanobacterial transcriptional activator NtcA. devH transcripts are barely detectable in vegetative cells and are induced approximately fivefold after nitrogen starvation. This induction is absent in the two developmental mutants hetR and ntcA. The gene is expressed as monocistronic transcripts with multiple 5' termini, and the approximately 500-bp region 5' to devH was shown to have promoter activity in vivo. The devH gene was insertionally inactivated by the integration of plasmid sequences within the open reading frame. Nitrogen starvation of the devH mutant induces heterocysts of wild-type morphology, but the mutant is inviable in the absence of fixed nitrogen and unable to reduce acetylene aerobically.
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PMID:Characterization of devH, a gene encoding a putative DNA binding protein required for heterocyst function in Anabaena sp. strain PCC 7120. 1085 91

The trxA gene encoding one of the different thioredoxins of the facultative heterotrophic cyanobacterium Synechocystis sp. PCC 6803 is transcribed as a single mRNA of 450 nucleotides. Transcript accumulation is similar in all standard growth conditions but strongly decreases after transferring cell cultures from light to darkness. In steady-state conditions, trxA transcription is reduced at high (150-500 microE m(-2) s(-1)) compared with moderate (10-50 microE m(-2) s(-1)) light intensities. The stability of the trxA transcript was similar at different light intensities, and also in darkness. Photosynthetic electron transport inhibitors, as well as glucose starvation in a mutant strain lacking photosystem II, promote a strong decline in the level of trxA transcript. Primer extension analysis suggests that trxA is transcribed from two proximal promoters containing a -10 TATA box similar to the Escherichia coli consensus promoters. Unlike the trxA mRNA, the amount of thioredoxin protein was not reduced in the dark, neither at high light intensities, indicating that thioredoxin protein is very stable. Our results indicate that the thioredoxin encoded by the trxA gene is likely to be primarily regulated at the transcriptional level, rather than at the protein level, by the electron transport generated photosynthetically or from glucose metabolism.
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PMID:Electron transport controls transcription of the thioredoxin gene (trxA) in the cyanobacterium Synechocystis sp. PCC 6803. 1094 71


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