scholarly journals H-NS is a part of a thermally controlled mechanism for bacterial gene regulation

2005 ◽  
Vol 391 (2) ◽  
pp. 203-213 ◽  
Author(s):  
Shusuke Ono ◽  
Martin D. Goldberg ◽  
Tjelvar Olsson ◽  
Diego Esposito ◽  
Jay C. D. Hinton ◽  
...  

Temperature is a primary environmental stress to which micro-organisms must be able to adapt and respond rapidly. Whereas some bacteria are restricted to specific niches and have limited abilities to survive changes in their environment, others, such as members of the Enterobacteriaceae, can withstand wide fluctuations in temperature. In addition to regulating cellular physiology, pathogenic bacteria use temperature as a cue for activating virulence gene expression. This work confirms that the nucleoid-associated protein H-NS (histone-like nucleoid structuring protein) is an essential component in thermoregulation of Salmonella. On increasing the temperature from 25 to 37 °C, more than 200 genes from Salmonella enterica serovar Typhimurium showed H-NS-dependent up-regulation. The thermal activation of gene expression is extremely rapid and change in temperature affects the DNA-binding properties of H-NS. The reduction in gene repression brought about by the increase in temperature is concomitant with a conformational change in the protein, resulting in the decrease in size of high-order oligomers and the appearance of increasing concentrations of discrete dimers of H-NS. The present study addresses one of the key complex mechanisms by which H-NS regulates gene expression.

2012 ◽  
Vol 80 (12) ◽  
pp. 4344-4353 ◽  
Author(s):  
Cristiano G. Moreira ◽  
Vanessa Sperandio

ABSTRACTThe bacterial adrenergic sensor kinases QseC and QseE respond to epinephrine and/or norepinephrine to initiate a complex phosphorelay regulatory cascade that modulates virulence gene expression in several pathogens. We have previously shown that QseC activates virulence gene expression inSalmonella entericaserovar Typhimurium. Here we report the role of QseE inS. Typhimurium pathogenesis as well as the interplay between these two histidine sensor kinases in gene regulation. AnS. TyphimuriumqseEmutant is hampered in the invasion of epithelial cells and intramacrophage replication. The ΔqseCstrain is highly attenuated for intramacrophage survival but has only a minor defect in invasion. However, the ΔqseECstrain has only a slight attenuation in invasion, mirroring the ΔqseCstrain, and has an intermediary intramacrophage replication defect in comparison to the ΔqseEand ΔqseCstrains. The expressions of thesipAandsopBgenes, involved in the invasion of epithelial cells, are activated by epinephrine via QseE. The expression levels of these genes are still decreased in the ΔqseECdouble mutant, albeit to a lesser extent, congruent with the invasion phenotype of this mutant. The expression level of thesifAgene, important for intramacrophage replication, is decreased in theqseEmutant and the ΔqseECdouble mutant grownin vitro. However, as previously reported by us, the epinephrine-dependent activation of this gene occurs via QseC. In the systemic model ofS. Typhimurium infection of BALB/c mice, theqseCandqseEmutants are highly attenuated, while the double mutant has an intermediary phenotype. Altogether, these data suggest that both adrenergic sensors play an important role in modulating several aspects ofS. Typhimurium pathogenesis.


2006 ◽  
Vol 188 (23) ◽  
pp. 8160-8168 ◽  
Author(s):  
Roberto Balbontín ◽  
Gary Rowley ◽  
M. Graciela Pucciarelli ◽  
Javier López-Garrido ◽  
Yvette Wormstone ◽  
...  

ABSTRACT Transcriptomic analyses during growth in Luria-Bertani medium were performed in strain SL1344 of Salmonella enterica serovar Typhimurium and in two isogenic derivatives lacking Dam methylase. More genes were repressed than were activated by Dam methylation (139 versus 37). Key genes that were differentially regulated by Dam methylation were verified independently. The largest classes of Dam-repressed genes included genes belonging to the SOS regulon, as previously described in Escherichia coli, and genes of the SOS-inducible Salmonella prophages ST64B, Gifsy-1, and Fels-2. Dam-dependent virulence-related genes were also identified. Invasion genes in pathogenicity island SPI-1 were activated by Dam methylation, while the fimbrial operon std was repressed by Dam methylation. Certain flagellar genes were repressed by Dam methylation, and Dam− mutants of S. enterica showed reduced motility. Altered expression patterns in the absence of Dam methylation were also found for the chemotaxis genes cheR (repressed by Dam) and STM3216 (activated by Dam) and for the Braun lipoprotein gene, lppB (activated by Dam). The requirement for DNA adenine methylation in the regulation of specific virulence genes suggests that certain defects of Salmonella Dam− mutants in the mouse model may be caused by altered patterns of gene expression.


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