Identification of transcription elements in the 5′ intergenic region shared by LON and MDJ1 heat shock genes from the human pathogen Paracoccidioides brasiliensis. Evaluation of gene expression

2007 ◽  
Vol 44 (5) ◽  
pp. 347-356 ◽  
Author(s):  
Wagner L. Batista ◽  
Tânia F. Barros ◽  
Gustavo H. Goldman ◽  
Flávia V. Morais ◽  
Rosana Puccia
Keyword(s):  
Gene Expression ◽  
Heat Shock ◽  
Intergenic Region ◽  
Paracoccidioides Brasiliensis ◽  
Human Pathogen ◽  
Heat Shock Genes

scholarly journals The hrcA and hspR regulons of Campylobacter jejuni

Microbiology ◽  
2010 ◽  
Vol 156 (1) ◽  
pp. 158-166 ◽  
Author(s):  
Christopher W. Holmes ◽  
Charles W. Penn ◽  
Peter A. Lund
Keyword(s):  
Gene Expression ◽  
Heat Shock ◽  
Campylobacter Jejuni ◽  
Growth Temperature ◽  
Heat Shock Response ◽  
Human Pathogen ◽  
Response Regulators ◽  
Heat Shock Genes ◽  
Shock Response ◽  
Number Of Genes

The human pathogen Campylobacter jejuni has a classic heat shock response, showing induction of chaperones and proteases plus several unidentified proteins in response to a small increase in growth temperature. The genome contains two homologues to known heat shock response regulators, HrcA and HspR. Previous work has shown that HspR controls several heat-shock genes, but the hrcA regulon has not been defined. We have constructed single and double deletions of C. jejuni hrcA and hspR and analysed gene expression using microarrays. Only a small number of genes are controlled by these two regulators, and the two regulons overlap. Strains mutated in hspR, but not those mutated in hrcA, showed enhanced thermotolerance. Some genes previously identified as being downregulated in a strain lacking hspR showed no change in expression in our experiments.

scholarly journals A Novel Mouse HSF3 Has the Potential to Activate Nonclassical Heat-Shock Genes during Heat Shock

2010 ◽  
Vol 21 (1) ◽  
pp. 106-116 ◽  
Author(s):  
Mitsuaki Fujimoto ◽  
Naoki Hayashida ◽  
Takuma Katoh ◽  
Kouji Oshima ◽  
Toyohide Shinkawa ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heat Shock ◽  
Cell Survival ◽  
Null Mouse ◽  
Wild Type ◽  
Heat Shock Genes ◽  
Embryonic Fibroblasts ◽  
Large Numbers ◽  
Inducible Genes ◽  
Transcription Factor 1

The heat-shock response is characterized by the expression of a set of classical heat-shock genes, and is regulated by heat-shock transcription factor 1 (HSF1) in mammals. However, comprehensive analyses of gene expression have revealed very large numbers of inducible genes in cells exposed to heat shock. It is believed that HSF1 is required for the heat-inducible expression of these genes although HSF2 and HSF4 modulate some of the gene expression. Here, we identified a novel mouse HSF3 (mHSF3) translocated into the nucleus during heat shock. However, mHSF3 did not activate classical heat-shock genes such as Hsp70. Remarkably, overexpression of mHSF3 restored the expression of nonclassical heat-shock genes such as PDZK3 and PROM2 in HSF1-null mouse embryonic fibroblasts (MEFs). Although down-regulation of mHSF3 expression had no effect on gene expression or cell survival in wild-type MEF cells, it abolished the moderate expression of PDZK3 mRNA and reduced cell survival in HSF1-null MEF cells during heat shock. We propose that mHSF3 represents a unique HSF that has the potential to activate only nonclassical heat-shock genes to protect cells from detrimental stresses.

scholarly journals Involvement of an ATP-Dependent Protease, PA0779/AsrA, in Inducing Heat Shock in Response to Tobramycin in Pseudomonas aeruginosa

2011 ◽  
Vol 55 (5) ◽  
pp. 1874-1882 ◽  
Author(s):  
Kristen N. Kindrachuk ◽  
Lucía Fernández ◽  
Manjeet Bains ◽  
Robert E. W. Hancock
Keyword(s):  
Gene Expression ◽  
Pseudomonas Aeruginosa ◽  
Heat Shock ◽  
Microarray Analysis ◽  
Prolonged Exposure ◽  
Short Term ◽  
Heat Shock Genes ◽  
Content Type ◽  
Expression Levels ◽  
Subinhibitory Concentrations

ABSTRACTThe adaptive resistance ofPseudomonas aeruginosato aminoglycosides is known to occur during chronic lung infections in cystic fibrosis patients in response to nonlethal concentrations of aminoglycosides. Not only is it difficult to achieve high levels of drug throughout the dehydrated mucus in the lung, but also steep oxygen gradients exist across the mucus layer, further reducing the bactericidal activity of aminoglycosides. In this study, microarray analysis was utilized to examine the gene responses ofP. aeruginosato lethal, inhibitory, and subinhibitory concentrations of tobramycin under aerobic and anaerobic conditions. While prolonged exposure to subinhibitory concentrations of tobramycin caused increased levels of expression predominantly of the efflux pump genesmexXY, the greatest increases in gene expression levels in response to lethal concentrations of tobramycin involved a number of heat shock genes and the PA0779 gene (renamed hereasrA), encoding an alternate Lon protease. Microarray analysis of anasrA::luxCDABEtransposon mutant revealed that the induction of heat shock genes in response to tobramycin in this mutant was significantly decreased compared to that in the parent strain. The level of expression ofasrAwas induced from an arabinose-inducible promoter to 35-fold greater than wild-type expression levels in the absence of tobramycin, and this overexpression alone caused an increased expression of the heat shock genes, as determined by quantitative PCR (qPCR). This overexpression ofasrAconferred short-term protection against lethal levels (4 μg/ml) of tobramycin but did not affect the tobramycin MIC. The RpoH heat shock sigma factor was found to be involved in the regulation ofasrAin response to both heat shock and tobramycin at the posttranscriptional level. The results of this work suggest that the tobramycin concentration has a significant impact on the gene expression ofP. aeruginosa, with lethal concentrations resulting in immediate adaptations conferring short-term protection, such as the induction of the heat shock response, and with subinhibitory concentrations leading to more sustainable long-term protection mechanisms, such as increased efflux.

CtsR controls class III heat shock gene expression in the human pathogen Listeria monocytogenes

2000 ◽  
Vol 35 (4) ◽  
pp. 800-811 ◽  
Author(s):  
Shamila Nair ◽  
Isabelle Derre ◽  
Tarek Msadek ◽  
Olivier Gaillot ◽  
Patrick Berche
Keyword(s):  
Gene Expression ◽  
Listeria Monocytogenes ◽  
Heat Shock ◽  
Heat Shock Gene ◽  
Human Pathogen ◽  
Class Iii ◽  
Shock Gene ◽  
Heat Shock Gene Expression

Hepatic Heat Shock and Acute-phase Gene Expression Are Induced Simultaneously after Celiotomy in the Anesthetized Pig

1995 ◽  
Vol 83 (4) ◽  
pp. 850-859. ◽  
Author(s):  
Benedikt H. J. Pannen ◽  
Kaori Maeda ◽  
Takao Ayuse ◽  
Nicola Brienza ◽  
Jean-Pierre Revelly ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heat Shock ◽  
Gene Transcription ◽  
Acute Phase ◽  
Acute Phase Reactant ◽  
Sodium Pentobarbital ◽  
Liver Ischemia ◽  
Heat Shock Genes ◽  
Phase Reactant ◽  
Rna Levels

Background The liver plays a central role in the whole organism's response to injury. Expression of hepatic acute-phase and heat-shock genes likely contributes to the restoration of homeostasis after stressful events. However, after prolonged ischemia, hepatic transcription of heat-shock genes can exclude the simultaneous transcription of acute-phase genes. The issue of whether hepatic 72-kd heat-shock protein (hsp72) gene expression is induced under perioperative conditions that do not result in prolonged liver ischemia and whether this might further affect the expression of the acute-phase reactant inter-alpha-trypsin inhibitor (alpha-Ti) was examined. Methods Pigs were anesthetized with sodium pentobarbital and ketamine hydrochloride, tracheally intubated, and their lungs ventilated. After celiotomy, a hepatic biopsy sample was obtained. Arterial blood pressure, cardiac output, and total hepatic blood flow were measured. Subsequent biopsies were obtained at 1, 2, 3, 4, and 6 h after the initial biopsy. Arterial norepinephrine concentrations were measured using high-pressure liquid chromatography. Nuclear runoff (run on) analysis and Northern blotting were applied to estimate changes in hsp72 and alpha-Ti gene transcription rates and RNA levels. Western blotting was used to estimate changes in hsp72 levels. Results Hemodynamic parameters did not change significantly over time. Arterial norepinephrine concentrations were increased at all time points. Hepatic hsp72 RNA levels increased up to sixfold while nuclear runoff assays did not detect significant changes in hsp72 gene transcription rates. The increases in hsp72 RNA levels correlated with accumulation of hsp72 (up to sevenfold). Increases in alpha-Ti transcription rates up to 42-fold were associated with respective increases in alpha-Ti RNA levels (up to 17-fold). Conclusions These data demonstrate that hepatic expression of hsp72 is not confined to conditions that lead to prolonged liver ischemia but is also part of the response of the liver to surgery under general anesthesia. Furthermore, these conditions are permissive for the simultaneous RNA expression of the acute-phase reactant alpha-Ti.

Induction of heat shock response leads to apoptosis in endothelial cells previously exposed to endotoxin

1993 ◽  
Vol 265 (1) ◽  
pp. H165-H170 ◽  
Author(s):  
T. G. Buchman ◽  
P. A. Abello ◽  
E. H. Smith ◽  
G. B. Bulkley
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Heat Shock ◽  
Acute Phase ◽  
Heat Shock Response ◽  
Acute Phase Response ◽  
Phase Response ◽  
Heat Shock Gene ◽  
Heat Shock Genes ◽  
Shock Response

The homeostatic response of complex eukaryotes to the challenge of environmental stress includes the induction of several programs of gene expression; among them are those for the acute phase genes and those for the heat shock genes. In some systems, the heat shock response, which is often elicited by more severe stimuli, preempts the acute phase response, which is seen in response to less severe challenges, as well as constitutive gene expression. Nevertheless, each response appears to provide a natural selective advantage for survival of the organism in a toxic environment. However, when cultured porcine endothelial cells were exposed first to a nonlethal level of bacterial endotoxin lipopolysaccharide (LPS), an inducer of the acute phase response, and then, simultaneously to standard stimuli, which normally elicit a salutary heat shock response, the cells died manifesting a pattern of DNA fragmentation (nucleolysis) characteristic of programmed cell death (apoptosis). The treatment of LPS-exposed cells with cycloheximide to block protein synthesis reproduced the lethal apoptosis that had been elicited by the induction of heat shock gene expression. Therefore, the preemption of other programs of stress gene expression by the prioritized expression of heat shock genes is associated with apoptosis.

Expression of Stress and Virulence Genes in Escherichia coli O157:H7 Heat Shocked in Fresh Dairy Compost

2015 ◽  
Vol 78 (1) ◽  
pp. 31-41 ◽  
Author(s):  
RANDHIR SINGH ◽  
XIUPING JIANG
Keyword(s):  
Gene Expression ◽  
Escherichia Coli ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Virulence Genes ◽  
Toxin Gene ◽  
Escherichia Coli O157 ◽  
Heat Shock Genes ◽  
E Coli ◽  
Shock Response

The purpose of this study was to determine the gene expression of Escherichia coli O157:H7 heat shocked in dairy compost. A two-step real-time PCR assay was used to evaluate the expression of stress and virulence genes in E. coli O157:H7 heat shocked in compost at 47.5°C for 10 min. Heat-shocked E. coli O157:H7 in compost was isolated by using an immunomagnetic bead separation method, followed by total RNA extraction, which was then converted to cDNA by using a commercial kit. E. coli O157:H7 heat shocked in broth served as the media control. In compost, heat shock genes (clpB, dnaK, and groEL) and the alternative sigma factor (rpoH) of E. coli O157:H7 were upregulated (P < 0.05), whereas the expression of trehalose synthesis genes did not change. Virulence genes, such as stx1 and fliC, were upregulated, while genes stx2, eaeA, and hlyA were down-regulated. In the toxin-antitoxin (TA) system, toxin genes, mazF, hipA, and yafQ were upregulated, whereas among antitoxin genes, only dinJ was upregulated (P < 0.05). In tryptic soy broth, all heat shock genes (rpoH, clpB, dnaK, and groEL) were upregulated (P < 0.05), and most virulence genes (stx1, stx2, hlyA, and fliC) and TA genes (mazF-mazE, hipA-hipB, and yafQ-dinJ and toxin gene chpS) were down-regulated. Our results revealed various gene expression patterns when E. coli O157:H7 inoculated in compost was exposed to a sublethal temperature. Clearly, induction of the heat shock response is one of the important protective mechanisms that prolongs the survival of pathogens during the composting process. In addition, other possible mechanisms (such as the TA system) operating along with heat shock response may be responsible for the extended survival of pathogens in compost.

scholarly journals Differential Gene Expression To Investigate the Effect of (5Z)-4-Bromo- 5-(Bromomethylene)-3-Butyl-2(5H)-Furanone on Bacillus subtilis

2004 ◽  
Vol 70 (8) ◽  
pp. 4941-4949 ◽  
Author(s):  
Dacheng Ren ◽  
Laura A. Bedzyk ◽  
Peter Setlow ◽  
Dacre F. England ◽  
Staffan Kjelleberg ◽  
...  
Keyword(s):  
Gene Expression ◽  
Bacillus Subtilis ◽  
Heat Shock ◽  
Stress Responses ◽  
Fatty Acid Biosynthesis ◽  
Expression Profiles ◽  
Test Organism ◽  
Class Iii ◽  
Heat Shock Genes ◽  
Gram Positive

ABSTRACT (5Z)-4-Bromo-5-(bromomethylene)-3-butyl-2(5H)-furanone (furanone) from the red marine alga Delisea pulchra was found previously to inhibit the growth, swarming, and biofilm formation of gram-positive bacteria. Using the gram-positive bacterium Bacillus subtilis as a test organism, we observed cell killing by 20 μg of furanone per ml, while 5 μg of furanone per ml inhibited growth approximately twofold without killing the cells. To discover the mechanism of this inhibition on a genetic level and to investigate furanone as a novel antibiotic, full-genome DNA microarrays were used to analyze the gene expression profiles of B. subtilis grown with and without 5 μg of furanone per ml. This agent induced 92 genes more than fivefold (P < 0.05) and repressed 15 genes more than fivefold (P < 0.05). The induced genes include genes involved in stress responses (such as the class III heat shock genes clpC, clpE, and ctsR and the class I heat shock genes groES, but no class II or IV heat shock genes), fatty acid biosynthesis, lichenan degradation, transport, and metabolism, as well as 59 genes with unknown functions. The microarray results for four genes were confirmed by RNA dot blotting. Mutation of a stress response gene, clpC, caused B. subtilis to be much more sensitive to 5 μg of furanone per ml (there was no growth in 8 h, while the wild-type strain grew to the stationary phase in 8 h) and confirmed the importance of the induction of this gene as identified by the microarray analysis.

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