<i>Listeria monocytogenes</i>10403S HtrA Is Necessary for Resistance to Cellular Stress and Virulence

Wilson, Rebecca L.; Brown, Lindsay L.; Kirkwood-Watts, Dana L.; Warren, Travis K.; Lund, Susan Amanda; King, David S.; Jones, Kevin F.; Hruby, Dennis E.

doi:10.1128/iai.74.1.765-768.2006

Cited by 74 publications

(76 citation statements)

References 28 publications

(25 reference statements)

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“…Thus, the cell envelope stress response of L. monocytogenes appears to be activated at multiple stages of the infectious process. In accordance with this, LisRK, CesRK and VirRS have been shown to contribute to pathogenesis in mice, and several of the genes shown to be highly upregulated in response to cefuroxime exposure play important roles in virulence, including dacA, lmo2714, htrA and the dlt-operon (Abachin et al, 2002;Camejo et al, 2009;Stack et al, 2005;Wilson et al, 2006;Woodward et al, 2010).…”

Section: Discussionmentioning

confidence: 89%

“…Furthermore, the expression of the htrA gene (lmo0292) encoding the serine protease HtrA, was induced 18-fold by cefuroxime exposure, corresponding to the third most upregulated gene in this study (Supplementary Table S2). HtrA is important for growth under stress conditions and contributes to virulence in L. monocytogenes (Stack et al, 2005;Wilson et al, 2006;Wonderling et al, 2004).…”

Section: Below)mentioning

confidence: 99%

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Genome-wide transcriptional profiling of the cell envelope stress response and the role of LisRK and CesRK in Listeria monocytogenes

et al. 2012

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The Gram-positive bacterium Listeria monocytogenes is widely distributed in the environment and capable of causing food-borne infections in susceptible individuals. In this study, we investigated the cell envelope stress response in L. monocytogenes. Whole-genome transcriptional profiling was performed to investigate the response upon exposure to the cell wall antibiotic cefuroxime. Differential expression (at least twofold) of 558 genes was observed, corresponding to 20 % of the L. monocytogenes genome. The majority of genes that were strongly induced by cefuroxime exposure have cell-envelope-related functions, including the dlt operon and the gene encoding penicillin-binding protein PBPD2. A large overlap was observed between the cefuroxime stimulon and genes known to be induced in L. monocytogenes in blood and during intracellular infection, indicating that the cell envelope stress response is active at various stages of the infectious process. We analysed the roles of the two-component systems LisRK and CesRK in the cell envelope response, showing that activation of the most highly cefuroxime-induced genes was LisR-and CesR-dependent. In addition, multiple VirRS-and LiaSR-regulated genes were found to be induced in response to cefuroxime exposure. In total, 53 % of the genes upregulated at least fourfold by cefuroxime exposure are under positive control by one of the four two-component systems. Using genetic analyses, we showed that several genes of the cefuroxime stimulon contribute to the innate resistance of L. monocytogenes to cefuroxime and tolerance to other cellenvelope-perturbing conditions. Collectively, these findings demonstrate central roles for twocomponent systems in orchestrating the cell envelope stress response in L. monocytogenes. INTRODUCTIONListeria monocytogenes is a Gram-positive, food-borne intracellular pathogen, causing life-threatening infections in susceptible individuals (Vázquez-Boland et al., 2001). L. monocytogenes is able to survive and propagate within many different environments, including soil, food processing environments, the gastrointestinal tract and the cytosol of mammalian cells. In order to adapt and multiply within such diverse and changing surroundings, L. monocytogenes must continuously monitor and respond to environmental signals by means of complex gene regulatory networks that coordinate the expression of specific sets of genes supporting bacterial survival and growth. The genome of L. monocytogenes encodes 14 two-component signal transduction systems and a single orphan response regulator which are thought to contribute to the coordinated response to various 3Present address: Molecular Genetics Group, Groningen Biomolecular Sciences and Biotechnology Institute, University of Groningen, Nijenborgh 7, 9747 AG Groningen, The Netherlands. The microarrays used in this study were generated and designed as described by van der Veen et al. (2010) (GEO Platform no. GPL14687) and the microarray data from this study have been deposited in the GEO database with accession...

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Section: Discussionmentioning

confidence: 89%

Section: Below)mentioning

confidence: 99%

Genome-wide transcriptional profiling of the cell envelope stress response and the role of LisRK and CesRK in Listeria monocytogenes

et al. 2012

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“…In L. monocytogenes, nine orthologues of these genes showed induction, including htrA. Other research has shown that HtrA is important for survival during exposure to environmental and cellular stresses (Stack et al, 2005;Wilson et al, 2006).…”

Section: Discussionmentioning

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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“…In bacteria, HtrA-like family members have been shown to participate in stress response networks, including those regulated through sigma factors and two-component systems (1,7). A subset of HtrA family members is also required for aspects of pathogenesis in both Gram-positive and Gramnegative organisms (14,16,45,49,57). M. tuberculosis possesses three HtrA-like proteases: Rv1223 (degP or htrA1), Rv0983 (pepD or htrA2), and Rv0215 (pepA or htrA3) (8,33), all of which share regions of sequence homology with one another.…”

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PepD Participates in the Mycobacterial Stress Response Mediated through MprAB and SigE

White

Penoske

et al. 2010

J Bacteriol

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Currently, one-third of the world's population is believed to be latently infected with Mycobacterium tuberculosis. The mechanisms by which M. tuberculosis establishes latent infection remain largely undefined. mprAB encodes a two-component signal transduction system required by M. tuberculosis for aspects of persistent infection. MprAB regulates a large and diverse group of genetic determinants in response to membrane stress, including the extracytoplasmic function (ECF) sigma factor sigE and the HtrA-like serine protease pepD. Recent studies have demonstrated that PepD functions as both a protease and chaperone in vitro. In addition, inactivation of pepD alters the virulence of M. tuberculosis in a mouse model system of infection. Here, we demonstrate that PepD plays an important role in the stress response network of Mycobacterium mediated through MprAB and SigE. In particular, we demonstrate that the protease activity of PepD requires the PDZ domain, in addition to the catalytic serine at position 317. pepD expression initiates from at least three promoters in M. tuberculosis, including one that is regulated by SigE and is located upstream of the mprA coding sequence. Deletion of pepD or mprAB in Mycobacterium smegmatis and M. tuberculosis alters the stress response phenotypes of these strains, including increasing sensitivity to SDS and cell wall antibiotics and upregulating the expression of stress-responsive determinants, including sigE. Taking these data together, we hypothesize that PepD utilizes its PDZ domain to recognize and process misfolded proteins at the cell membrane, leading to activation of the MprAB and SigE signaling pathways and subsequent establishment of a positive feedback loop that facilitates bacterial adaptation.Currently, one-third of the world's population is believed to be latently infected with Mycobacterium tuberculosis, the causative agent of tuberculosis. There are an estimated 9 million new cases of infection caused by this organism each year, accounting for more than 2 million deaths annually (3). This makes M. tuberculosis one of the leading causes of death due to a single infectious agent. Humans are the only known reservoir of M. tuberculosis, and as such, part of its success as a pathogen lies in its ability to maintain a significant persistent reservoir within the population. Latently infected individuals are asymptomatic and are harder to treat, thereby complicating measures to control the spread of disease (27). In addition, the emergence of multi-and extensively drug-resistant strains has further compromised established strategies for treatment. A better understanding of the mechanisms by which M. tuberculosis establishes persistent infection is urgently needed so that better therapeutics for the latently infected population can be developed.M. tuberculosis is a facultative intracellular pathogen that primarily infects alveolar macrophages. The organism survives within these cells by blocking key steps in the phagosome maturation process (38). Infection by M. tubercul...

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Listeria monocytogenes10403S HtrA Is Necessary for Resistance to Cellular Stress and Virulence

Cited by 74 publications

References 28 publications

Genome-wide transcriptional profiling of the cell envelope stress response and the role of LisRK and CesRK in Listeria monocytogenes

Genome-wide transcriptional profiling of the cell envelope stress response and the role of LisRK and CesRK in Listeria monocytogenes

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

PepD Participates in the Mycobacterial Stress Response Mediated through MprAB and SigE

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