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

The study of plant ribonuclease (RNase) functions is complicated by a complex profile of RNase activities detected in tissues. Thus, isolation of individual RNase genes will be desirable for the further understanding of function of each RNase. Here, we describe the isolation of cDNAs encoding two RNases, ZRNaseI and ZRNaseII, in differentiating tracheary elements (TEs) induced from isolated mesophyll cells of Zinnia elegans. Both the ZRNaseI and ZRNaseII exhibit putative secretion signal sequences at the amino-terminal ends with predicted molecular masses of 24 247 Da and 22 448 Da as mature proteins, respectively. DNA gel blot analysis showed that both RNases in Zinnia appear to be encoded by a small gene family. RNA gel blot analysis showed that the expression of the ZRNaseI gene was associated with the late stage of in vitro TE differentiation, whereas the ZRNaseII gene was mainly induced in response to stress. Neither RNase gene was induced in response to phosphate starvation, or to H2O2 challenge in the cultured mesophyll cells, or to senescence in the leaves. In young leaves, the ZRNaseI gene was not induced in response to wounding. But the ZRNaseII gene was markedly induced by 6 h after wounding. Tissue print hybridization showed that the expression of the ZRNaseI gene was preferentially associated with the differentiation TEs in Zinnia stems, while the ZRNaseII mRNA was not detected in unwounded Zinnia organs. Taken together, the results indicated that the ZRNaseI gene is expressed during the process of xylogenesis both in vitro and in the plant, whereas the ZRNaseII gene is predominantly induced in response to wounding. The identification of these RNase genes provides molecular tools for the dissection of the process of autolysis during xylogenesis, and for the dissection of the role of RNase in wounding response.
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PMID:Isolation and characterization of cDNAs encoding xylogenesis-associated and wounding-induced ribonucleases in Zinnia elegans. 862 3

The starvation-stress response (SSR) of Salmonella typhimurium encompasses the physiological changes that occur upon starvation for an essential nutrient, e.g. C-source. A subset of SSR genes, known as core SSR genes, are required for the long-term starvation survival of the bacteria. Four core SSR loci have been identified in S. typhimurium: rpoS, stiA, stiB, and stiC. Here we report that in S. typhimurium C-starvation induced a greater and more sustainable cross-resistance to oxidative challenge (15 mM hydrogen peroxide (H2O2) for 40 min) than either N- or P-starvation. Of the four core SSR loci, only rpoS and stiC mutants exhibited a defective C-starvation-inducible cross-resistance to H2O2 challenge. Interestingly, (unadapted) log-phase S. typhimurium rpoS and stiA mutants were very sensitive to oxidative challenge. Based on this, we determined if these core SSR loci were important for H2O2 resistance developed during a 60 min adaptive exposure to 60 microM H2O2 (adapted cells). Both unadapted and adapted rpoS and stiA mutants were hypersensitive to a H2O2 challenge. In addition, a stiB mutant exhibited normal adaptive resistance for the first 20 mins of H2O2 challenge but then rapidly lost viability, declining to a level of about 1.5% of the wild-type strain. The results of these experiments indicate that: (i) the rpoS and stiC loci are essential for the development of C-starvation-inducible cross-resistance to oxidative challenge, and (ii) the rpoS, stiA, and, in a delayed effect, stiB loci are needed for H2O2-inducible adaptive resistance to oxidative challenge. Moreover, we found that both stiA and stiB are induced by a 60 microM H2O2 exposure, but only stiA was regulated (repressed) by (reduced form) OxyR.
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PMID:Essential roles of core starvation-stress response loci in carbon-starvation-inducible cross-resistance and hydrogen peroxide-inducible adaptive resistance to oxidative challenge in Salmonella typhimurium. 873 29

Compared with growing bacteria, carbohydrate-starved cells of Enterococcus faecalis show development of a multiresistance state against heat, H2O2, acid, and ethanol, but not against UV irradiation. The kinetics of acquisition of resistance is different according to the stress. Three hours of starvation provide maximal resistance against ethanol, while the tolerance to heat, H2O2, and acid increases progressively with the duration of starvation. Chloramphenicol treatment does not abolish the ethanol tolerance. Protein synthesis inhibition during the transitional growth phase and the first hours of starvation partially inhibit the acquisition of heat and oxidative resistances. Antibiotic treatment after 3 h of starvation does not affect the increase of these resistances. We suggest that synthesis of specific proteins revealed by 2-D gel analysis in the first 3 h of starvation, followed by a second mechanism related to protein degradation or alteration, is necessary for acquisition of maximal resistance towards heat and oxidative stresses.
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PMID:Starvation-induced multiresistance in Enterococcus faecalis JH2-2. 885 73

We have investigated the mechanisms of killing of Escherichia coli by HOCl by identifying protective functions. HOCl challenges were performed on cultures arrested in stationary phase and in exponential phase. Resistance to HOCl in both cases was largely mediated by genes involved in resistance to hydrogen peroxide (H2O2). In stationary phase, a mutation in rpoS, which controls the expression of starvation genes including those which protect against oxidative stress, renders the cells hypersensitive to killing by HOCl. RpoS-regulated genes responsible for this sensitivity were dps, which encodes a DNA-binding protein, and, to a lesser extent, katE and katG, encoding catalases; all three are involved in resistance to H2O2. In exponential phase, induction of the oxyR regulon, an adaptive response to H2O2, protected against HOCl exposure, and the oxyR2 constitutive mutant is more resistant than the wild-type strain. The genes involved in this oxyR-dependent resistance have not yet been identified, but they differ from those primarily involved in resistance to H2O2, including katG, ahp, and dps. Pretreatment with HOCl conferred resistance to H2O2 in an OxyR-independent manner, suggesting a specific adaptive response to HOCl. fur mutants, which have an intracellular iron overload, were more sensitive to HOCl, supporting the generation of hydroxyl radicals upon HOCl exposure via a Fenton-type reaction. Mutations in recombinational repair genes (recA or recB) increased sensitivity to HOCl, indicative of DNA strand breaks. Sensitivity was visible in the wild type only at concentrations above 0.6 mg/liter, but it was observed at much lower concentrations in dps recA mutants.
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PMID:Hypochlorous acid stress in Escherichia coli: resistance, DNA damage, and comparison with hydrogen peroxide stress. 889 12

A sublethal dose of ethanol (5%, vol/vol), acid (HCl, pH 4.5 to 5.0), H2O2 (500 ppm), or NaCl (7%, wt/vol) was added to a Listeria monocytogenes culture at the exponential phase, and the cells were allowed to grow for 1 h. Exponential-phase cells also were heat shocked at 45 degrees C for 1 h. The stress-adapted cells were then subjected to the following factors at the indicated lethal levels--NaCl (25%, wt/vol), ethanol (17.5%, vol/vol), hydrogen peroxide (0.1%, wt/vol), acid (pH 3.5), and starvation on 0.1 M phosphate buffer at pH 7.0 (up to 300 h). Viable counts of the pathogen, after the treatment, were determined on Trypticase soy agar-yeast extract, and survivor plots were constructed. The area (h.log10 CFU/ml) between the control and treatment curves was calculated to represent the protective effect resulting from adaptation to the sublethal stress factor. Adaptation to pH 4.5 to 5.0 or 5% ethanol significantly (P < 0.05) increased the resistance of L. monocytogenes to lethal doses of acid, ethanol, and H2O2. Adaptation to ethanol significantly (P < 0.05) increased the resistance to 25% NaCl. When L. monocytogenes was adapted to 500 ppm of H2O2, 7% NaCl, or heat, resistance of the pathogen to 1% hydrogen peroxide increased significantly (P < 0.05). Heat shock significantly (P < 0.05) increased the resistance to ethanol and NaCl. Therefore, the occurrence of stress protection after adaptation of L. monocytogenes to environmental stresses depends on the type of stress encountered and the lethal factor applied. This "stress hardening" should be considered when current food processing technologies are modified or new ones are developed.
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PMID:Adaptation to sublethal environmental stresses protects Listeria monocytogenes against lethal preservation factors. 909 20

Mycobactericum smegmatis ATCC 607 became iron starved and did not reach maximum population density when grown at an iron concentration of 0.1 microM, or less. Iron deficient cells were more susceptible than iron replete cells to H2O2 killing; 9 mM H2O2 killed about 80% of the population of cultures grown at 0.05 microM iron, while about 25 mM H2O2 was required for similar killing of cultures grown at 1 or 20 microM iron. In response to H2O2, iron sufficient cells produced major oxidative stress proteins of molecular masses of 90, 75, 65, 62, and 43 kDa (the 75 and 65 kDa proteins were identified as DnaK and GroEL homologs, respectively). Iron deficient M. smegmatis did not upregulate the DnaK and GroEL proteins when stressed with H2O2. Both iron deficient and iron sufficient M. smegmatis produced (at 48 degrees C) major heat shock proteins of molecular masses of 90, 75 (DnaK), 65 (GroEL), 62, 43, and 16 kDa. The stress protein response induced by 2 M ethanol challenge was similar to the heat shock response except that ethanol induced a unique 55 kDa protein and the 16 kDa heat shock protein was not apparent. Induction of ethanol stress proteins was identical in high iron and low iron cells. All of the stress agents induced expression of a 62 kDa protein which may also be induced by iron insufficiency. The heat and ethanol shock responses of M. smegmatis were unchanged by iron deficiency; therefore, the absence of DnaK and GroEL from the response of iron starved M. smegmatis to H2O2 may be due to a specific defect (or alteration) of the oxidative stress response during iron starvation.
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PMID:Enhanced hydrogen peroxide sensitivity and altered stress protein expression in iron-starved Mycobacterium smegmatis. 924 99

The ability of cells to survive freezing and thawing is expected to depend on the physiological conditions experienced prior to freezing. We examined factors affecting yeast cell survival during freeze-thaw stress, including those associated with growth phase, requirement for mitochondrial functions, and prior stress treatment(s), and the role played by relevant signal transduction pathways. The yeast Saccharomyces cerevisiae was frozen at -20 degrees C for 2 h (cooling rate, less than 4 degrees C min-1) and thawed on ice for 40 min. Supercooling occurred without reducing cell survival and was followed by freezing. Loss of viability was proportional to the freezing duration, indicating that freezing is the main determinant of freeze-thaw damage. Regardless of the carbon source used, the wild-type strain and an isogenic petite mutant ([rho 0]) showed the same pattern of freeze-thaw tolerance throughout growth, i.e., high resistance during lag phase and low resistance during log phase, indicating that the response to freeze-thaw stress is growth phase specific and not controlled by glucose repression. In addition, respiratory ability and functional mitochondria are necessary to confer full resistance to freeze-thaw stress. Both nitrogen and carbon source starvation led to freeze-thaw tolerance. The use of strains affected in the RAS-cyclic AMP (RAS-cAMP) pathway or supplementation of an rca1 mutant (defective in the cAMP phosphodiesterase gene) with cAMP showed that the freeze-thaw response of yeast is under the control of the RAS-cAMP pathway. Yeast did not adapt to freeze-thaw stress following repeated freeze-thaw treatment with or without a recovery period between freeze-thaw cycles, nor could it adapt following pretreatment by cold shock. However, freeze-thaw tolerance of yeast cells was induced during fermentative and respiratory growth by pretreatment with H2O2, cycloheximide, mild heat shock, or NaCl, indicating that cross protection between freeze-thaw stress and a limited number of other types of stress exists.
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PMID:The freeze-thaw stress response of the yeast Saccharomyces cerevisiae is growth phase specific and is controlled by nutritional state via the RAS-cyclic AMP signal transduction pathway. 932 44

SigmaB-dependent general stress proteins (Gsps) of Bacillus subtilis are essential for the development of glucose-starvation-induced cross-resistance to oxidative challenge. However, the proteins directly involved in this nonspecific resistance to oxidative stress have to be identified. We found that one prominent Gsp displayed strong sequence similarity to the previously characterized oxidative-stress-inducible MrgA protein of B. subtilis and to the starvation-induced Dps/PexB protein of Escherichia coli. We therefore designated this prominent Gsp Dps. While MrgA belongs to the peroxide-stress-inducible proteins needed for the H2O2-inducible adaptive response to oxidative stress, Dps belongs to the proteins induced by heat, salt, or ethanol stress and after starvation for glucose but not by a sublethal oxidative challenge. Primer extension experiments identified two overlapping promoters upstream of the coding region of dps, one being sigmaB dependent (PB) and the other being sigmaB independent (P1). Both promoters contribute to the basal level of dps during growth. After stress or during entry into the stationary phase, transcription from PB strongly increased whereas transcription from P1 decreased. Mutant strains lacking Dps completely failed to develop glucose-starvation-induced resistance to oxidative stress. These results confirm our suggestion that sigmaB-dependent general stress proteins of B. subtilis are absolutely required for the development of nonspecific resistance to oxidative stress.
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PMID:Expression of a stress- and starvation-induced dps/pexB-homologous gene is controlled by the alternative sigma factor sigmaB in Bacillus subtilis. 939 87

A mitogen-activated protein kinase (MAPK) has been cloned and sequenced from a Drosophila neoplasmic l(2)mbn cell line. The cDNA sequence analysis showed that this Drosophila kinase is a homologue of mammalian p38 MAPK and the yeast HOG1 gene and thus was referred to as Dp38. A distinguishing feature of all MAPKs is the conserved sequence TGY in the activation domain. Dp38 was rapidly tyrosine 186-phosphorylated in response to osmotic stress, heat shock, serum starvation, and H2O2 in Drosophila l(2)mbn and Schneider cell lines. However, unlike mammalian p38 MAPK, the addition of lipopolysaccharide (LPS) did not significantly affect the phosphorylation of Dp38 in the LPS-responsive l(2)mbn cell line. Following osmotic stress, tyrosine 186-phosphorylated forms of Dp38 MAPK were detected exclusively in nuclear regions of Schneider cells. Yeast complementation studies demonstrated that the Saccharomyces cerevisiae HOG1 mutant strain JBY10 (hog1-Delta1) was functionally complemented by Dp38 cDNA in hyperosmolar medium. These findings demonstrate that similar osmotic stress-responsive signal transduction pathways are conserved in yeast, Drosophila, and mammalian cells, whereas LPS signal transduction pathways appear to be different.
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PMID:Molecular cloning and characterization of a Drosophila p38 mitogen-activated protein kinase. 941 90

Nucleotide sequence of Xanthomonas oryzae pv. oryzae (Xoo) DNA from pSM-A1 was determined and sequence analysis revealed an ORF with high homology to RecA proteins. Expression analysis using an anti-RecA antibody demonstrates that MMS treatment induces recA in Xanthomonas strains but not in an Escherichia coli harbouring cloned Xoo recA. This indicates the existence of a recA regulatory mechanism in Xanthomonas that is not function in E. coli. In Xoo, recA was highly induced by treatments with chemical mutagens, UV and peroxides, while superoxides, a thiol agent, a heavy metal and heat shock were not inducers. The increased amount of RecA induced by H2O2 or MMS treatments were due to increased transcription of recA. recA showed no growth phase or starvation regulation. The pattern of recA regulation in Xoo could play important roles in stress survival in the environment and during plant-microbe interactions.
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PMID:Characterization and expression analysis of a Xanthomonas oryzae pv. oryzae recA. 946 92


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