The RNA-binding protein PNPase regulates biofilm formation and virulence in Listeria monocytogenes
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ABSTRACT:
PROVIDER: PRJNA863648 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20715593_1.fastq.gz | Fastqsanger.gz | |||
| SRR20715593_2.fastq.gz | Fastqsanger.gz | |||
| SRR20715594_1.fastq.gz | Fastqsanger.gz | |||
| SRR20715594_2.fastq.gz | Fastqsanger.gz | |||
| SRR20715595_1.fastq.gz | Fastqsanger.gz |
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Project description:Biofilm-related diseases are typically persistent infections, and a challenge for medical treatment. Biofilms are communities of bacteria that attach to surfaces and are enclosed in an extracellular matrix. These sessile microorganisms can endure external stresses like nutrient deprivation, antibiotic treatments, and immune defences. Therefore, biofilms create conditions favourable for bacterial pathogenesis. The knowledge of novel biofilm regulators may contribute to develop new strategies to fight microbial infections. In this work we study the role of the RNA-binding protein and RNA-degradative enzyme polynucleotide phosphorylase (PNPase) from the human pathogen Listeria monocytogenes. We show that inactivation of Listeria PNPase not only leads to strong defects in biofilm production, but also affects biofilm morphology. RNA-seq analysis of the RNA extracted from biofilms of the wild-type and the PNPase mutant strains revealed major changes in the expression of genes affecting the metabolism of carbon. Lastly, infection assays in eukaryotic cell lines confirmed that PNPase deletion leads to the severe attenuation of Listeria monocytogenes pathogenicity. Overall, our results show that PNPase is a novel regulator of biofilm formation and human cellular invasion of a bacterial pathogen. This work presents PNPase as a new and attractive target for the control of bacterial infection and highlights the expanding role of RNA-binding proteins as critical players in pathogenicity.
2023-06-05 | GSE210097 | GEO
Project description:The formation of Listeria monocytogenes biofilms contributes to persistent contamination in food processing facilities. A microarray comparison of L. monocytogenes between the transcriptome of the strong biofilm forming strain (Bfms) Scott A and the weak biofilm forming (Bfmw) strain F2365 was conducted to identify genes potentially involved in biofilm formation. Among 951 genes with significant difference in expression between the two strains, a GntR-family response regulator encoding gene (LMOf2365_0414), designated lbrA, was found to be highly expressed in Scott A relative to F2365. A Scott A lbrA-deletion mutant, designated AW3, formed biofilm to a much lesser extent as compared to the parent strain by a rapid attachment assay and scanning electron microscopy. Complementation with lbrA from Scott A restored the Bfms phenotype in the AW3 derivative. A second microarray assessment using the lbrA deletion mutant AW3 and the wild type Scott A revealed a total of 304 genes with expression significantly different between the two strains, indicating the potential regulatory role of LbrA in L. monocytogenes. A cloned copy of Scott A lbrA was unable to confer enhanced biofilm forming potential in F2365, suggesting that additional factors contributed to weak biofilm formation by F2365. Findings from the study may lead to new strategies to modulate biofilm formation. Two comparisons were performed between 1) strong biofilm former Listeria monocytogenes strain ScottA versus weak biofilm former Listeria monocytogenes strain F2365; 2) Listeria monocytogenes ScottA LbrA deletion mutant strain versus Listeria monocytogenes ScottA. Four replicates were loaded for the first comparison and two replicates were loaded for the second comparison.
2012-09-06 | E-GEOD-40598 | biostudies-arrayexpress
Project description:Exploiting genomic differences between Listeria monocytogenes EGDe isolates reveals crucial roles for SigB and wall rhamnosylation in biofilm formation.
2019-11-18 | PRJEB35335 | EVA
Project description:External signals are key for bacteria to sense their immediate environment and fine-tune gene expression accordingly. The foodborne pathogen Listeria monocytogenes senses a range of environmental cues in order to activate or deactivate the virulence-inducing transcriptional factor PrfA during transition between infectious and saprophytic lifecycles. Chitin is an abundant biopolymer formed from linked β-(1–4)-N-acetyl-D-glucosamine residues associated with fungi, the exoskeleton of insects and often incorporated into foods as a thickener or stabiliser. L. monocytogenes evolved to hydrolyse chitin, presumably, to facilitate nutrient acquisition from competitive environments such as soil where the polymer is abundant. Since mammals do not produce chitin, we reasoned that the polymer could serve as an environmental signal contributing to repression of L. monocytogenes PrfA-dependent expression outside the host. This study shows a significant downregulation of the core PrfA-regulon during virulence-inducing conditions in vitro in the presence of chitin. Our data suggest this phenomenon occurs through a mechanism that differs from PTS-transport of oligosaccharides generated from either degradation or chitinase-mediated hydrolysis of the polymer. Importantly, an indication that chitin can repress virulence expression of a constitutively active PrfA* mutant is shown, possibly mediated via a post-translational modification inhibiting PrfA* activity. To our knowledge, chitin as a molecule with anti-virulence properties against a pathogenic bacterium has not been previously reported. Thus, our findings identify chitin as a signal which may downregulate the virulence potential of the pathogen and may provide an alternative approach towards reducing disease risk.
2020-12-22 | GSE154844 | GEO
Project description:The foodborne pathogen Listeria monocytogenes has the ability to develop biofilm in food-processing environment, which becomes a major concern for the food safety. PrfA, a key transcriptional activator that regulates most of the known listerial virulence gene expression, has been shown to promote L. monocytogenes biofilm formation. In this study, the whole genome microarray was used to identify differentially expressed genes associated with the putative interaction between biofilm formation and PrfA in L. monocytogenes. Comparative transcriptome analyses indicated over 21.9% of the L. monocytogenes EGDe genes (627 out of 2857 predicted) were altered in their expression in biofilm cells relative to planktonic cell populations. These genes were classed into different functional categories which cover most of the biochemical functions encountered in bacterial cells, especially involved in ion transport, DNA repair, and cell wall biosynthesis based on significant enrichment of GO terms. Among them, 185 genes were identified to be associated with PrfA and biofilm formation by comparison of the whole gene expression profiles of L. monocytogenes EGDe and its M-NM-^TprfA mutant. The expression tendency of these PrfA-associated and biofilm-specific genes were mainly opposite in M-NM-^TprfA biofilm, and most of them are involved in phage-related function, membrane bioenergetics, and cell wall. Our results indicated that L. monocytogenes biofilm formation is probably controlled by the complex regulation network involved variable genes required for the different biological pathways. This regulatory network is modified in the prfA deletion mutant in order to maintain its stable biofilm lifestyle. Gene expression of planktonic cells and biofilm cells in Listeria monocytogenes EGDe and prfA isogenic deletion strain EGDeM-NM-^TprfA with cultivated in MEM and BHI for 48 hours, were mesasued using Agilent Listeria monocytogenes customized whole-genome microarray 8x15 array. Three replicates.
2013-05-01 | E-GEOD-43052 | biostudies-arrayexpress
Project description:For bacteria in general and Listeria monocytogenes in particular, little is known about transcriptome diversity in comparison to the copious data on intraspecific genome diversity. The current study employed RNA sequencing to investigate the variation of transcript levels of conserved single copy genes from several perspectives including differences between lineages and correlation with previous classification of the virulence potential of clonal complexes based on epidemiological MLST data. Infection of G. mellonella, a surrogate host, also allowed a correlation analysis with virulence data experimentally determined in vivo.
2019-09-10 | GSE129537 | GEO
Project description:Persistence of Listeria monocytogenes in retail deli environments is a serious food safety issue, potentially leading to cross-contamination of ready-to-eat foods such as deli meats, salads, and cheeses. We previously discovered strong evidence of L. monocytogenes persistence in delis across multiple states. We hypothesized that this was correlated with isolates’ innate characteristics, such as biofilm-forming capacity or gene differences.We further chose four isolates for RNA-sequencing analysis and compared their global biofilm transcriptome to their global planktonic transcriptome. Analysis of biofilm vs planktonic gene expression did not show the expected differences in gene expression patterns. Overall, L. monocytogenes persistence in the deli environment is likely a matter of poor sanitation and/or facility design, rather than isolates’ biofilm-forming capacity, sanitizer tolerance, or genomic content
2021-06-11 | GSE176617 | GEO
Project description:The foodborne pathogen Listeria monocytogenes (Lm) can cause invasive infection in susceptible animals and humans. To survive and proliferate within hosts, this facultative intracellular pathogen needs to tightly coordinate the expression of a complex regulatory network, including virulence factors. Here, we identify and characterize MouR a novel virulence regulator of Lm. Through RNA-seq transcriptomic analysis, we characterized the MouR regulatory network and demonstrated how MouR positively controls the expression of the Agr system (agrBDCA) of Lm. Resolving MouR 3D structure revealed a dimeric DNA-binding transcription factor belonging to the VanR class of the GntR superfamily of regulatory proteins. We showed that by direct binding to the agr promoter region, MouR ultimately modulates chitinase activity and biofilm formation. Importantly, we demonstrated by in vitro cell invasion assays and in vivo mice infections the crucial role of MouR for Lm full virulence.
2018-10-22 | GSE106833 | GEO
Project description:The formation of Listeria monocytogenes biofilms contributes to persistent contamination in food processing facilities. A microarray comparison of L. monocytogenes between the transcriptome of the strong biofilm forming strain (Bfms) Scott A and the weak biofilm forming (Bfmw) strain F2365 was conducted to identify genes potentially involved in biofilm formation. Among 951 genes with significant difference in expression between the two strains, a GntR-family response regulator encoding gene (LMOf2365_0414), designated lbrA, was found to be highly expressed in Scott A relative to F2365. A Scott A lbrA-deletion mutant, designated AW3, formed biofilm to a much lesser extent as compared to the parent strain by a rapid attachment assay and scanning electron microscopy. Complementation with lbrA from Scott A restored the Bfms phenotype in the AW3 derivative. A second microarray assessment using the lbrA deletion mutant AW3 and the wild type Scott A revealed a total of 304 genes with expression significantly different between the two strains, indicating the potential regulatory role of LbrA in L. monocytogenes. A cloned copy of Scott A lbrA was unable to confer enhanced biofilm forming potential in F2365, suggesting that additional factors contributed to weak biofilm formation by F2365. Findings from the study may lead to new strategies to modulate biofilm formation.
2012-09-06 | GSE40598 | GEO
Project description:Listeria monocytogenes SigB and PrfA are pleiotropic regulators of stress response and virulence gene expression, which have been shown to co-regulate genes in L. monocytogenes. We performed whole genome transcriptional profiling in the presence of PrfA* and active SigB, to identify the overlaps between the PrfA virulence regulon and the SigB stress response regulon. In L. monocytogenes, the PrfA* allele contributes to the activation of virulence genes to a level comparable to that of intracellular growing L. monocytogenes. Our results showed that the core PrfA regulon consists of 12 genes previously described as PrfA regulated. Furthermore, we found that the role of SigB during virulence gene regulation changes, dependent on the presence or absence of PrfA*. In the absence of PrfA*, SigB activated the transcription of virulence genes such as inlA and inlB. In the presence of PrfA*, SigB negatively influenced the transcription of genes in the PrfA core regulon. The observed effect of SigB on the transcript level of PrfA regulated genes was shown to reduce the cytotoxic effect of the PrfA* allele in HepG-2 cells. Our results indicate that the SigB-PrfA regulatory network is important for the adjustment of virulence gene transcription to ensure L. monocytogenes success as an intracellular pathogen. Keywords: comparison of gene expression of regulatory mutants
2008-10-01 | GSE11347 | GEO