SigB-Dependent In Vitro Transcription of<i>prfA</i>and Some Newly Identified Genes of<i>Listeria monocytogenes</i>Whose Expression Is Affected by PrfA In Vivo

Rauch, Marcus; Luo, Qiong; Müller-Altrock, Stefanie; Goebel, Werner

doi:10.1128/jb.187.2.800-804.2005

Cited by 68 publications

(72 citation statements)

References 28 publications

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“…Accordingly, numerous PrfA-regulated virulence genes (Milohanic et al, 2003) showed upregulation after heat exposure, including plcA (lmo0201), encoding a phospholipase, inlA and inlB (lmo0433 and lmo0434), encoding Listeria-specific internalins, lmo2067, encoding a conjugated bile acid hydrolase, and lmo0596, encoding an unknown protein. However, Rauch et al (2005) have shown that PrfA has no direct influence on the transcription of lmo2067 and lmo0596. Significant down-regulation was found for the agr locus (lmo0048-lmo0051).…”

Section: Virulence-associated Genesmentioning

confidence: 99%

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

et al. 2007

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The food-borne pathogen Listeria monocytogenes has the ability to survive extreme environmental conditions due to an extensive interacting network of stress responses. It is able to grow and survive at relatively high temperatures in comparison with other non-sporulating food-borne pathogens. To investigate the heat-shock response of L. monocytogenes, whole-genome expression profiles of cells that were grown at 37 6C and exposed to 48 6C were examined using DNA microarrays. Transcription levels were measured over a 40 min period after exposure of the culture to 48 6C and compared with those of unexposed cultures at 37 6C. After 3 min, 25 % of all genes were differentially expressed, while after 40 min only 2 % of all genes showed differential expression, indicative of the transient nature of the heat-shock response. The global transcriptional response was validated by analysing the expression of a set of 13 genes by quantitative PCR. Genes previously identified as part of the class I and class III heat-shock response and the class II stress response showed induction at one or more of the time points investigated. This is believed to be the first study to report that several heat-shock-induced genes are part of the SOS response in L. monocytogenes. Furthermore, numerous differentially expressed genes that have roles in the cell division machinery or cell wall synthesis were down-regulated. This expression pattern is in line with the observation that heat shock results in cell elongation and prevention of cell division.

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Section: Virulence-associated Genesmentioning

confidence: 99%

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

et al. 2007

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“…Furthermore in silico search revealed additional genes which contain in their upstream non-coding and hence probably regulatory regions sequences similar to PrfAbinding sites (PrfA-boxes) found in the well-established PrfA-dependent promoters of virulence genes of L. monocytogenes . However, neither in vivo nor in vitro transcription studies could demonstrate the direct involvement of PrfA in the transcription of these latter genes (Milohanic et al, 2003;Rauch et al, 2005). Thus, neither method has delivered reliable results concerning bona fide new PrfA- Fig.…”

Section: Discussionmentioning

confidence: 99%

“…Some of these sequences were tested for PrfA-dependent promoter activity in the in vitro transcription assay (Rauch et al, 2005). None of these tested putative promoters responded to PrfA.…”

Section: Figmentioning

confidence: 99%

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Supportive and inhibitory elements of a putative PrfA‐dependent promoter inListeria monocytogenes

Luo

Herler

Müller-Altrock

et al. 2005

Molecular Microbiology

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SummaryElements essential for PrfA-dependent transcription were analysed on two promoters of Listeria monocytogenes , the PrfA-dependent promoter of the phospholipase gene plcA (P plcA ) and a putative promoter of the aroA gene (P aroA2 ) which contains a similar PrfA-binding site and a similar ----10 box as P plcA but does not function as PrfA-dependent promoter. We constructed a series of hybrid plcA-aroA promoters by exchanging corresponding sequence elements of these two 'promoters'. The results showed that the two critical elements of PrfA-dependent promoters, the PrfA-box and the ----10 box, can be functionally exchanged as long as the distance in between is maintained to 22 or 23 bp. However, the interspace sequence and the sequence downstream of the ----10 box of P aroA2 were strongly inhibitory for PrfAdependent transcription. A detailed analysis of these two sequences revealed that the RNA polymerase binding site being part of the actual in vivo and in vitro used aroA promoter (P aroA1 ) and a sequence immediately downstream of the putative ----10 site, possibly blocking the formation of the open complex, were responsible for the inhibition of PrfA-dependent transcription from P aroA2 . Taking into consideration the lessons learned from this study we were able to construct a functional PrfA-dependent aroA promoter.

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“…The significance of this operon as a central mechanism in the sophisticated adaptive mechanisms to stress has been highlighted in a wide range of bacteria (Karlin et al, 2004;Satorhelyi, 2004). In L. monocytogenes, it is involved in resistance against alkali, oxidative, osmotic, heat, bile, and acid stress (Ferreira et al, 2004;Moorhead and Dykes, 2004;Sue et al, 2004;Giotis et al, 2008a) and is also important in virulence and the ability to invade host cells (Kim et al, 2005;Rauch et al, 2005;Garner et al, 2006). As might be expected of such an important regulon, sigB is itself subject to a complex regulatory system, and this study observed that AS induced significant upregulation of three genes (lmo0889, lmo0891, and lmo0892) that encode for proteins involved in the regulation of sigB.…”

Section: Adaptive Mechanismsmentioning

confidence: 99%

Transcriptome Analysis of Alkali Shock and Alkali Adaptation inListeria monocytogenes10403S

Giotis

Muthaiyan

Natesan

et al. 2010

Foodborne Pathogens and Disease

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Alkali stress is an important means of inactivating undesirable pathogens in a wide range of situations. Unfortunately, Listeria monocytogenes can launch an alkaline tolerance response, significantly increasing persistence of the pathogen in such environments. This study compared transcriptome patterns of alkali and nonalkalistressed L. monocytogenes 10403S cells, to elucidate the mechanisms by which Listeria adapts and=or grows during short-or long-term alkali stress. Transcription profiles associated with alkali shock (AS) were obtained by DNA microarray analysis of midexponential cells suspended in pH 9 media for 15, 30, or 60 min. Transcription profiles associated with alkali adaptation (AA) were obtained similarly from cells grown to midexponential phase at pH 9. Comparison of AS and AA transcription profiles with control cell profiles identified a high number of differentially regulated open-reading frames in all tested conditions. Rapid (15 min) changes in expression included upregulation of genes encoding for multiple metabolic pathways (including those associated with Na + =H + antiporters), ATP-binding cassette transporters of functional compatible solutes, motility, and virulence-associated genes as well as the s B controlled stress resistance network. Slower (30 min and more) responses to AS and adaptation during growth in alkaline conditions (AA) involved a different pattern of changes in mRNA concentrations, and genes involved in proton export.

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SigB-Dependent In Vitro Transcription ofprfAand Some Newly Identified Genes ofListeria monocytogenesWhose Expression Is Affected by PrfA In Vivo

Cited by 68 publications

References 28 publications

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

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

Supportive and inhibitory elements of a putative PrfA‐dependent promoter inListeria monocytogenes

Transcriptome Analysis of Alkali Shock and Alkali Adaptation inListeria monocytogenes10403S

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