scholarly journals HrcA and DnaK are important for static and continuous-flow biofilm formation and disinfectant resistance in Listeria monocytogenes

Microbiology ◽  
2010 ◽  
Vol 156 (12) ◽  
pp. 3782-3790 ◽  
Author(s):  
Stijn van der Veen ◽  
Tjakko Abee
Keyword(s):  
Listeria Monocytogenes ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Peracetic Acid ◽  
Continuous Flow ◽  
Biofilm Formation ◽  
Benzalkonium Chloride ◽  
Wild Type ◽  
Shock Response ◽  
Disinfectant Resistance

The food-borne pathogen Listeria monocytogenes is able to form biofilms in food processing environments. Since biofilms are generally difficult to eradicate during clean-up procedures, they pose a major risk for the food industry. Stress resistance mechanisms involved in L. monocytogenes biofilm formation and disinfectant resistance have, to our knowledge, not been identified thus far. In this study, we investigated the role of hrcA, which encodes the transcriptional regulator of the class I heat-shock response, and dnaK, which encodes a class I heat-shock response chaperone protein, in static and continuous-flow biofilm formation and resistance against benzalkonium chloride and peracetic acid. Induction of both hrcA and dnaK during continuous-flow biofilm formation was observed using quantitative real-time PCR and promoter reporters. Furthermore, in-frame deletion and complementation mutants of hrcA and dnaK revealed that HrcA and DnaK are required to reach wild-type levels of both static and continuous-flow biofilms. Finally, disinfection treatments of planktonic-grown cells and suspended static and continuous-flow biofilm cells of wild-type and mutants showed that HrcA and DnaK are important for resistance against benzalkonium chloride and peracetic acid. In conclusion, our study revealed that HrcA and DnaK are important for L. monocytogenes biofilm formation and disinfectant resistance.

scholarly journals Importance of SigB for Listeria monocytogenes Static and Continuous-Flow Biofilm Formation and Disinfectant Resistance

2010 ◽  
Vol 76 (23) ◽  
pp. 7854-7860 ◽  
Author(s):  
Stijn van der Veen ◽  
Tjakko Abee
Keyword(s):  
Listeria Monocytogenes ◽  
Peracetic Acid ◽  
Continuous Flow ◽  
Biofilm Formation ◽  
Benzalkonium Chloride ◽  
Antimicrobial Agents ◽  
Resistance Mechanisms ◽  
Stress Response Genes ◽  
Food Borne

ABSTRACT Listeria monocytogenes is a food-borne pathogen that is able to form biofilms in food processing facilities. Biofilms are generally more resistant to antimicrobial agents, making it difficult to eradicate them during cleanup procedures. So far, little is known about the function of stress resistance mechanisms in biofilm formation and their resistance to disinfectants. In this study, we investigated the role of sigB, which encodes a major transcriptional regulator of stress response genes, in L. monocytogenes static and continuous-flow biofilm formation and its function in the resistance of biofilm cells to the disinfectants benzalkonium chloride and peracetic acid. Quantitative real-time PCR and promoter reporter studies showed that sigB is activated in static and continuous-flow biofilms. Biofilm formation studies using an in-frame sigB deletion mutant and complementation mutant showed that the presence of SigB is required to obtain wild-type levels of both static and continuous-flow biofilms. Finally, disinfection treatments of planktonically grown cells and cells dispersed from static and continuous-flow biofilms showed that SigB is involved in the resistance of both planktonic cells and biofilms to the disinfectants benzalkonium chloride and peracetic acid.

scholarly journals The heat-shock response of Listeria monocytogenes comprises genes involved in heat shock, cell division, cell wall synthesis, and the SOS response

Microbiology ◽  
2007 ◽  
Vol 153 (10) ◽  
pp. 3593-3607 ◽  
Author(s):  
Stijn van der Veen ◽  
Torsten Hain ◽  
Jeroen A. Wouters ◽  
Hamid Hossain ◽  
Willem M. de Vos ◽  
...  
Keyword(s):  
Cell Wall ◽  
Cell Division ◽  
Listeria Monocytogenes ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Sos Response ◽  
Cell Wall Synthesis ◽  
Shock Cell ◽  
Shock Response ◽  
Division Cell

scholarly journals Acyadeletion mutant ofEscherichia colidevelops thermotolerance but does not exhibit a heat-shock response

1990 ◽  
Vol 55 (1) ◽  
pp. 1-6 ◽  
Author(s):  
John M. Delaney
Keyword(s):  
Protein Synthesis ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Heat Shock Response ◽  
Receptor Protein ◽  
Wild Type ◽  
E Coli ◽  
Shock Response ◽  
In The Wild ◽  
Shock Proteins

SummaryAn adenyl cyclase deletion mutant (cya) ofE. colifailed to exhibit a heat-shock response even after 30 min at 42 °C. Under these conditions, heat-shock protein synthesis was induced by 10 min in the wild-type strain. These results suggest that synthesis of heat-shock proteins inE. colirequires thecyagene. This hypothesis is supported by the finding that a presumptive cyclic AMP receptor protein (CRP) binding site exists within the promotor region of theE. coli htp Rgene. In spite of the absence of heat-shock protein synthesis, when treated at 50 °C, thecyamutant is relatively more heat resistant than wild type. Furthermore, when heat shocked at 42 °C prior to exposure at 50 °C, thecyamutant developed thermotolerance. These results suggest that heat-shock protein synthesis is not essential for development of thermotolerance inE. coli.

scholarly journals Metabolic Roles of a Rhodobacter sphaeroides Member of the ς32 Family

1998 ◽  
Vol 180 (1) ◽  
pp. 10-19 ◽  
Author(s):  
Russell K. Karls ◽  
Jacqueline Brooks ◽  
Peter Rossmeissl ◽  
Janelle Luedke ◽  
Timothy J. Donohue
Keyword(s):  
Heat Shock ◽  
Temperature Profile ◽  
Rhodobacter Sphaeroides ◽  
Growth Temperature ◽  
Heat Shock Response ◽  
Anaerobic Respiration ◽  
Wild Type ◽  
Lower Growth ◽  
E Coli ◽  
Shock Response

ABSTRACT We report the role of a gene (rpoH) from the facultative phototroph Rhodobacter sphaeroides that encodes a protein (ς37) similar to Escherichia coliς32 and other members of the heat shock family of eubacterial sigma factors. R. sphaeroides ς37controls genes that function during environmental stress, since anR. sphaeroides ΔRpoH mutant is ∼30-fold more sensitive to the toxic oxyanion tellurite than wild-type cells. However, the ΔRpoH mutant lacks several phenotypes characteristic of E. coli cells lacking ς32. For example, anR. sphaeroides ΔRpoH mutant is not generally defective in phage morphogenesis, since it plates the lytic virus RS1, as well as its wild-type parent. In characterizing the response ofR. sphaeroides to heat, we found that its growth temperature profile is different when cells generate energy by aerobic respiration, anaerobic respiration, or photosynthesis. However, growth of the ΔRpoH mutant is comparable to that of a wild-type strain under each of these conditions. The ΔRpoH mutant mounted a heat shock response when aerobically grown cells were shifted from 30 to 42°C, but it exhibited altered induction kinetics of ∼120-, 85-, 75-, and 65-kDa proteins. There was also reduced accumulation of several presumed heat shock transcripts (rpoD PHS,groESL 1, etc.) when aerobically grown ΔRpoH cells were placed at 42°C. Under aerobic conditions, it appears that another sigma factor enables the ΔRpoH mutant to mount a heat shock response, since either RNA polymerase preparations from an ΔRpoH mutant, reconstituted Eς37, or a holoenzyme containing a 38-kDa protein (ς38) each transcribed E. coliEς32-dependent promoters. The lower growth temperature profile of photosynthetic cells is correlated with a difference in heat-inducible gene expression, since neither wild-type cells or the ΔRpoH mutant mount a typical heat shock response after such cultures were shifted from 30 to 37°C.

Evidence for a role of heat shock factor 1 in inhibition of NF-κB pathway during heat shock response-mediated lung protection

2004 ◽  
Vol 287 (5) ◽  
pp. L953-L961 ◽  
Author(s):  
Delphine Wirth ◽  
Fabrice Bureau ◽  
Dorothée Melotte ◽  
Elisabeth Christians ◽  
Pascal Gustin
Keyword(s):  
Heat Shock ◽  
Heat Shock Response ◽  
Weight Ratio ◽  
Lung Damage ◽  
Central Component ◽  
Wild Type ◽  
Lung Protection ◽  
Gm Csf ◽  
Shock Response

Heat shock transcription factor (HSF)-1 is recognized as a central component of the heat shock response, which protects against various harmful conditions. However, the mechanisms underlying the protection and the role of HSF-1 in these mechanisms have not yet been clearly elucidated. Using HSF-1 knockout mice ( Hsf1−/−), we examined whether heat shock response-mediated lung protection involved an inhibition of the proinflammatory pathway via an interaction between HSF-1 and NF-κB, in response to cadmium insult. The HSF-1-dependent protective effect against intranasal instillation of cadmium (10 and 100 μg/mouse) was demonstrated by the higher protein content (1.2- and 1.4-fold), macrophage (1.6- and 1.9-fold), and neutrophil (2.6- and 1.8-fold) number in bronchoalveolar fluids, higher lung wet-to-dry weight ratio, and more severe lung damage evaluated by histopathology in Hsf1−/− compared with wild-type animals. These responses were associated with higher granulocyte/macrophage colony-stimulating factor (GM-CSF; 1.7-fold) but not TNF-α concentrations in bronchoalveolar fluids of Hsf1−/− mice compared with those of wild-type animals, indicating that HSF-1 behaved as a repressor of specific cytokine production in our model. To further investigate the mechanism of GM-CSF repression, we analyzed the NF-κB activity and IκB stability. The DNA binding NF-κB activity, in particular p50 homodimer activity, was higher in Hsf1−/− mice than in wild-type mice after cadmium exposure. These results provide a first line of evidence that mechanisms of lung protection depending on HSF-1 involve specific cytokine repression via inhibition of NF-κB activation in vivo.

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