scholarly journals Convergence of Molecular, Modeling, and Systems Approaches for an Understanding of the Escherichia coli Heat Shock Response

2008 ◽  
Vol 72 (3) ◽  
pp. 545-554 ◽  
Author(s):  
Eric Guisbert ◽  
Takashi Yura ◽  
Virgil A. Rhodius ◽  
Carol A. Gross
Keyword(s):  
Escherichia Coli ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Feedback Loop ◽  
Model Organism ◽  
Central Component ◽  
E Coli ◽  
Functional Aspects ◽  
Shock Response ◽  
Homeostatic Response

SUMMARY The heat shock response (HSR) is a homeostatic response that maintains the proper protein-folding environment in the cell. This response is universal, and many of its components are well conserved from bacteria to humans. In this review, we focus on the regulation of one of the most well-characterized HSRs, that of Escherichia coli. We show that even for this simple model organism, we still do not fully understand the central component of heat shock regulation, a chaperone-mediated negative feedback loop. In addition, we review other components that contribute to the regulation of the HSR in E. coli and discuss how these additional components contribute to regulation. Finally, we discuss recent genomic experiments that reveal additional functional aspects of the HSR.

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.

The efficacy of long-lasting residual drinking water disinfectants based on hydrogen peroxide and silver

2000 ◽  
Vol 42 (1-2) ◽  
pp. 293-298 ◽  
Author(s):  
R. Pedahzur ◽  
D. Katzenelson ◽  
N. Barnea ◽  
O. Lev ◽  
H.I. Shuval ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Heat Shock ◽  
Stress Responses ◽  
Heat Shock Response ◽  
Chemical Properties ◽  
Bactericidal Effect ◽  
Physiological Effects ◽  
Mechanisms Of Toxicity ◽  
E Coli ◽  
Shock Response

The aim of the present work was to evaluate the disinfectant capacity and the possible fields of application of a combined silver and hydrogen peroxide (HP) water disinfectant. The findings demonstrated the high bactericidal action of silver (on E. coli) and its relatively ineffective virucidal effect (on MS-2 phage). HP was found to have a small bactericidal effect and a mild virucidal one. When combined, silver and HP usually exhibited a synergistic action on the viability of E. coli and on the luminescence of recombinant luminescent E. coli. In some instances, the combined bactericidal effects were 1000-fold higher than the sum of the separate ones. No increased virucidal action was observed. The biocidal action of the combination generally increased with increasing temperature and pH, and decreased in secondary and tertiary effluents. The physiological effects and mechanisms of toxicity of HP, silver and their combinations, were assessed by monitoring the induction of stress promoters upon exposure to the active agents, and by assessing the sensitivity of E. coli mutated in major stress responses to HP, silver and their combinations. The results showed that HP induced a wide array of stress responses, that both silver and HP induced promoters regulated by the heat shock response, and that the dnaK promoter (regulated by the heat shock response) was synergistically induced. The mutant sensitivity tests showed that bacteria deficient in the ability to activate central cellular stress responses (SOS, heat shock, stationary phase, oxidative) were hypersensitive to both HP and silver. These results imply that cellular proteins, and possibly the DNA, are the cellular moieties chiefly affected. The above findings suggest that the potentiated effect of HP and silver is a metabolically dependant/related process that stems from a combination and/or accumulation of physiological effects exerted by the active ingredients. The physico-chemical properties of the combined disinfectant, and its disinfection capacity, points to its potential application as a long-term secondary residual disinfectant for water of relatively high quality.

The heat shock response of E. coli is regulated by changes in the concentration of σ32

Nature ◽  
1987 ◽  
Vol 329 (6137) ◽  
pp. 348-351 ◽  
Author(s):  
David B. Straus ◽  
William A. Walter ◽  
Carol A. Gross
Keyword(s):  
Heat Shock ◽  
Heat Shock Response ◽  
E Coli ◽  
Shock Response

scholarly journals Heat shock response in Escherichia coli influences cell division.

1986 ◽  
Vol 83 (18) ◽  
pp. 6959-6963 ◽  
Author(s):  
T. Tsuchido ◽  
R. A. VanBogelen ◽  
F. C. Neidhardt
Keyword(s):  
Escherichia Coli ◽  
Cell Division ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Shock Response

scholarly journals An alkaline shift induces the heat shock response in Escherichia coli.

1987 ◽  
Vol 169 (2) ◽  
pp. 885-887 ◽  
Author(s):  
D Taglicht ◽  
E Padan ◽  
A B Oppenheim ◽  
S Schuldiner
Keyword(s):  
Escherichia Coli ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Alkaline Shift ◽  
Shock Response

Effect of Heat Shock and Incubation Atmosphere on Injury and Recovery of Escherichia coli O157:H7

1993 ◽  
Vol 56 (7) ◽  
pp. 568-572 ◽  
Author(s):  
ELSA A. MURANO ◽  
MERLE D. PIERSON
Keyword(s):  
Escherichia Coli ◽  
Heat Treatment ◽  
Heat Shock ◽  
Escherichia Coli O157 ◽  
Toxic Substances ◽  
Anaerobic Conditions ◽  
E Coli ◽  
Heat Treated ◽  
Shock Response ◽  
Cell Components

Escherichia coli serotype O157:H7 cells were grown at 30°C for 6 h and subjected to a heat stress, or heat shock, at 42°C for 5 min. Heat-shocked and nonheat-shocked controls were heat treated at 55°C for up to 60 min. The number of injured cells was significantly higher in heat-shocked cells than in controls, and the rate of release of cell components was higher in heat-shocked cells. Anaerobic plating resulted in higher recovery of injured cells, when compared with aerobic plating, regardless of whether the cells were heat shocked or not. In addition, heat shocking resulted in lower catalase and superoxide dismutase activities when compared with controls. It also resulted in greater survivability after exposure to hydrogen peroxide, suggesting that heat shocking somehow enables the cells to survive exposure to toxic substances in addition to heat. The heat-shock response, coupled with anaerobic conditions, increased the ability of E. coli O157:H7 cells to recover after a heat treatment. Thus, heat shock did not afford protection to the cells against injury, but rather enhanced their ability to recover during storage.

Sign in / Sign up

Export Citation Format

Share Document