scholarly journals Regulation of finP Transcription by DNA Adenine Methylation in the Virulence Plasmid of Salmonella enterica

2005 ◽  
Vol 187 (16) ◽  
pp. 5691-5699 ◽  
Author(s):  
Eva M. Camacho ◽  
Ana Serna ◽  
Cristina Madrid ◽  
Silvia Marqués ◽  
Raúl Fernández ◽  
...  

ABSTRACT DNA adenine methylase (Dam−) mutants of Salmonella enterica serovar Typhimurium contain reduced levels of FinP RNA encoded on the virulence plasmid. Dam methylation appears to regulate finP transcription, rather than FinP RNA stability or turnover. The finP promoter includes canonical −10 and −35 modules and depends on the σ70 factor. Regulation of finP transcription by Dam methylation does not require DNA sequences upstream from the −35 module, indicating that Dam acts at the promoter itself or downstream. Unexpectedly, a GATC site overlapping with the −10 module is likewise dispensable for Dam-mediated regulation. These observations indicate that Dam methylation regulates finP transcription indirectly and suggest the involvement of a host factor(s) responsive to the Dam methylation state of the cell. We provide evidence that one such factor is the nucleoid protein H-NS, which acts as a repressor of finP transcription in a Dam− background. H-NS also restrains transcription of the overlapping traJ gene, albeit in a Dam-independent fashion. Hence, the decreased FinP RNA content found in Dam− hosts of S. enterica appears to result from H-NS-mediated repression of finP transcription.

2008 ◽  
Vol 190 (22) ◽  
pp. 7406-7413 ◽  
Author(s):  
Marcello Jakomin ◽  
Daniela Chessa ◽  
Andreas J. Bäumler ◽  
Josep Casadesús

ABSTRACT DNA adenine methylase (dam) mutants of Salmonella enterica serovar Typhimurium grown under laboratory conditions express the std fimbrial operon, which is tightly repressed in the wild type. Here, we show that uncontrolled production of Std fimbriae in S. enterica serovar Typhimurium dam mutants contributes to attenuation in mice, as indicated by the observation that an stdA dam strain is more competitive than a dam strain upon oral infection. Dam methylation appears to regulate std transcription, rather than std mRNA stability or turnover. A genetic screen for std regulators showed that the GATC-binding protein SeqA directly or indirectly represses std expression, while the poorly characterized yifA gene product serves as an std activator. YifA encodes a putative LysR-like protein and has been renamed HdfR, like its Escherichia coli homolog. Activation of std expression by HdfR is observed only in dam and seqA backgrounds. These data suggest that HdfR directly or indirectly activates std transcription. Since SeqA is unable to bind nonmethylated DNA, it is possible that std operon derepression in dam and seqA mutants may result from unconstrained HdfR-mediated activation of std transcription. Derepression of std in dam and seqA mutants of S. enterica occurs in only a fraction of the bacterial population, suggesting the occurrence of either bistable expression or phase variation.


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.


Genetics ◽  
1999 ◽  
Vol 152 (1) ◽  
pp. 31-45 ◽  
Author(s):  
Joaquín Torreblanca ◽  
Silvia Marqués ◽  
Josep Casadesús

Abstract DNA adenine methylase mutants of Salmonella typhimurium contain reduced amounts of FinP, an antisense RNA encoded by the virulence plasmid pSLT. Lowered FinP levels are detected in both Dam- FinO+ and Dam- FinO- backgrounds, suggesting that Dam methylation regulates FinP production rather than FinP half-life. Reduced amounts of F-encoded FinP RNA are likewise found in Dam- mutants of Escherichia coli. A consequence of FinP RNA scarcity in the absence of DNA adenine methylation is that Dam- mutants of both S. typhimurium and E. coli show elevated levels of F plasmid transfer. Inhibition of F fertility by the S. typhimurium virulence plasmid is also impaired in a Dam- background.


2015 ◽  
Vol 77 (2) ◽  
pp. 181-186 ◽  
Author(s):  
Hidenori MATSUI ◽  
Yasunori ISSHIKI ◽  
Masahiro EGUCHI ◽  
Yohsuke OGAWA ◽  
Yoshihiro SHIMOJI

2001 ◽  
Vol 183 (15) ◽  
pp. 4652-4658 ◽  
Author(s):  
Hidenori Matsui ◽  
Christopher M. Bacot ◽  
Wendy A. Garlington ◽  
Thomas J. Doyle ◽  
Steve Roberts ◽  
...  

ABSTRACT In a mouse model of systemic infection, the spv genes carried on the Salmonella enterica serovar Typhimurium virulence plasmid increase the replication rate of salmonellae in host cells of the reticuloendothelial system, most likely within macrophages. A nonpolar deletion in the spvB gene greatly decreased virulence but could not be complemented by spvBalone. However, a low-copy-number plasmid expressing spvBCfrom a constitutive lacUV5 promoter did complement thespvB deletion. By examining a series of spvmutations and cloned spv sequences, we deduced thatspvB and spvC could be sufficient to confer plasmid-mediated virulence to S. enterica serovar Typhimurium. The spvBC-bearing plasmid was capable of replacing all of the spv genes, as well as the entire virulence plasmid, of serovar Typhimurium for causing systemic infection in BALB/c mice after subcutaneous, but not oral, inoculation. A point mutation in the spvBC plasmid preventing translation but not transcription of spvC eliminated the ability of the plasmid to confer virulence. Therefore, it appears that both spvB and spvC encode the principal effector factors for Spv- and plasmid-mediated virulence of serovar Typhimurium.


2016 ◽  
Vol 4 (2) ◽  
Author(s):  
Pablo Vinuesa ◽  
José L. Puente ◽  
Edmundo Calva ◽  
Mussaret B. Zaidi ◽  
Claudia Silva

The complete genome of Salmonella enterica serovar Typhimurium strain SO3 (sequence type 302), isolated from a fatal meningitis infection in Mexico, was determined using PacBio technology. The chromosome hosts six complete prophages and is predicted to harbor 51 genomic islands, including 13 pathogenicity islands (SPIs). It carries the Salmonella virulence plasmid (pSTV).


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