scholarly journals Genetic and phenotypic characterization of the heat shock response in Pseudomonas putida

2014 ◽  
Vol 3 (6) ◽  
pp. 922-936 ◽  
Author(s):  
Fumihiro Ito ◽  
Takayuki Tamiya ◽  
Iwao Ohtsu ◽  
Makoto Fujimura ◽  
Fumiyasu Fukumori
Author(s):  
Victor S. Wang ◽  
Nu Nu Kyin ◽  
Claire Pollock ◽  
Hyjoung Lee ◽  
Xin Li ◽  
...  

1995 ◽  
Vol 16 (4) ◽  
pp. 801-811 ◽  
Author(s):  
Gracjana Klein ◽  
Robert Walczak ◽  
Ewa Krasnowska ◽  
Adam Blaszczak ◽  
Barbara Lipińska

2012 ◽  
Vol 194 (9) ◽  
pp. 2342-2354 ◽  
Author(s):  
D. Apel ◽  
J. Ellermeier ◽  
M. Pryjma ◽  
V. J. DiRita ◽  
E. C. Gaynor

Microbiology ◽  
2005 ◽  
Vol 151 (3) ◽  
pp. 905-915 ◽  
Author(s):  
Marianne Thorup Andersen ◽  
Lone Brøndsted ◽  
Bruce M. Pearson ◽  
Francis Mulholland ◽  
Mary Parker ◽  
...  

Campylobacter jejuni is a leading cause of bacterial gastroenteritis in the developed world. The role of a homologue of the negative transcriptional regulatory protein HspR, which in other organisms participates in the control of the heat-shock response, was investigated. Following inactivation of hspR in C. jejuni, members of the HspR regulon were identified by DNA microarray transcript profiling. In agreement with the predicted role of HspR as a negative regulator of genes involved in the heat-shock response, it was observed that the transcript amounts of 13 genes were increased in the hspR mutant, including the chaperone genes dnaK, grpE and clpB, and a gene encoding the heat-shock regulator HrcA. Proteomic analysis also revealed increased synthesis of the heat-shock proteins DnaK, GrpE, GroEL and GroES in the absence of HspR. The altered expression of chaperones was accompanied by heat sensitivity, as the hspR mutant was unable to form colonies at 44 °C. Surprisingly, transcriptome analysis also revealed a group of 17 genes with lower transcript levels in the hspR mutant. Of these, eight were predicted to be involved in the formation of the flagella apparatus, and the decreased expression is likely to be responsible for the reduced motility and ability to autoagglutinate that was observed for hspR mutant cells. Electron micrographs showed that mutant cells were spiral-shaped and carried intact flagella, but were elongated compared to wild-type cells. The inactivation of hspR also reduced the ability of Campylobacter to adhere to and invade human epithelial INT-407 cells in vitro, possibly as a consequence of the reduced motility or lower expression of the flagellar export apparatus in hspR mutant cells. It was concluded that, in C. jejuni, HspR influences the expression of several genes that are likely to have an impact on the ability of the bacterium to successfully survive in food products and subsequently infect the consumer.


1989 ◽  
Vol 90 (3) ◽  
pp. 1156-1162 ◽  
Author(s):  
Stefan Moisyadi ◽  
H. Michael Harrington

1995 ◽  
Vol 177 (4) ◽  
pp. 932-937 ◽  
Author(s):  
J A Eastgate ◽  
N Taylor ◽  
M J Coleman ◽  
B Healy ◽  
L Thompson ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document