Role of the Dickeya dadantii PecS regulator during the early stages of plant infection
Ontology highlight
ABSTRACT:
ORGANISM(S): Dickeya dadantii 3937
PROVIDER: GSE94713 | GEO | 2017/02/10
SECONDARY ACCESSION(S): PRJNA373837
REPOSITORIES: GEO
Similar Datasets
Project description:Pathogenicity of the phytopathogenic enterobacterium Erwinia chrysanthemi, the causative agent of soft rot disease in many plants, is a complex process involving several factors whose production is subject to temporal regulation during infection. After penetrating into its host plant, E. chrysanthemi resides latently in the plant intercellular spaces without provoking any symptoms, and disease occurs only when the environmental conditions are favourable for massive bacterial multiplication and production of plant cell wall degrading enzymes. PecS is a transcriptional regulator of the MarR family that represses production of plant cell wall degrading enzymes. Here, we used microarray analysis to define the PecS regulon and demonstrated that PecS exerts wide-ranging effects on gene expression in E. chrysanthemi. However, the major effects of PecS are largely confined to specific genes that could be linked to pathogenicity and to a group of genes concerned with evading host defences. Among the identified targets are the genes encoding plant cell wall degrading enzymes, secretion systems, the genes involved in flagella synthesis, in biosurfactant synthesis, in oxidative stress response as well as genes encoding toxin-like virulence factors such as NipE and Hemolysin-coregulated proteins. Electromobility shift assays and DNAse I footprinting demonstrated that PecS directly interacts with the regulatory regions of five new targets, ahpC, rhlA, nipE, virK, avrL, that define three different functional classes of genes: oxidative stress response genes (ahpC), biosurfactant synthesis gene (rhlA), genes encoding exported proteins related to other plant associated bacteria proteins (nipE, virK, avrL). Based on this work, we propose a pivotal role of PecS in the switch from a saprophytic to a parasitic lifestyle.
2008-10-09 | E-TABM-428 | biostudies-arrayexpress
Project description:We report the characterization of the major regulator of virulence gene expression (CovR) in Group B Streptococcus. The ChIP-seq experiments define the binding of CovR on the chromosome of the BM110 strain, a representative of the hypervirulent GBS lineage responsible of neonatal meningitis. Regulatory evolution of CovR signaling was investigated by comparing ChIP-seq done in parallel in a second GBS clinical isolate (NEM316) not belonging to the hypervirulent lineage.
2021-08-23 | GSE158046 | GEO
Project description:PECs from wild-type, NF-IL6KO and KI(LAP) mice were stimulated with or without LPS+IFN-gamma for 12h. We used microarrays to check the difference of gene induction among wild type, KO and KI mice. Keywords: Wild, KO and KI(LAP)
2007-12-05 | GSE7649 | GEO
Project description:Many transcriptional regulators control gene activity by responding to specific ligands. Members of the multiple-antibiotic resistance regulator (MarR) family of transcriptional regulators feature prominently in this regard, and they frequently function as repressors in the absence of their cognate ligands. Plant pathogens such as Dickeya dadantii encode a MarR homolog named PecS that controls expression of a gene encoding the efflux pump PecM in addition to other virulence genes. We report here that the soil bacterium Streptomyces coelicolor also encodes a PecS homolog (SCO2647) that regulates a pecM gene (SCO2646). S. coelicolor PecS, which exists as a homodimer, binds the intergenic region between pecS and pecM genes with high affinity. Several potential PecS binding sites were found in this intergenic region. The binding of PecS to its target DNA can be efficiently attenuated by the ligand urate, which also quenches the intrinsic fluorescence of PecS, indicating a direct interaction between urate and PecS. In vivo measurement of gene expression showed that activity of pecS and pecM genes is significantly elevated after exposure of S. coelicolor cultures to urate. These results indicate that S. coelicolor PecS responds to the ligand urate by attenuated DNA binding in vitro and upregulation of gene activity in vivo. Since production of urate is associated with generation of reactive oxygen species by xanthine dehydrogenase, we propose that PecS functions under conditions of oxidative stress.
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Project description:PECs from wild-type, NF-IL6KO and KI(LAP) mice were stimulated with or without LPS+IFN-gamma for 12h. We used microarrays to check the difference of gene induction among wild type, KO and KI mice. Experiment Overall Design: Peritoneal macrophages were collected for RNA extraction and hybridization on Affymetrix microarrays.
2008-06-15 | E-GEOD-7649 | biostudies-arrayexpress
Project description:PecS is one of the major global regulators controlling the virulence of Dickeya dadantii, a broad-host-range phytopathogenic bacterium causing soft rot on several plant families. To define the PecS regulon during plant colonization, we analysed the global transcriptome profiles in wild-type and pecS mutant strains during the early colonization of the leaf surfaces and in leaf tissue just before the onset of symptoms, and found that the PecS regulon consists of more than 600 genes. About one-half of these genes are down-regulated in the pecS mutant; therefore, PecS has both positive and negative regulatory roles that may be direct or indirect. Indeed, PecS also controls the regulation of a few dozen regulatory genes, demonstrating that this global regulator is at or near the top of a major regulatory cascade governing adaptation to growth in planta. Notably, PecS acts mainly at the very beginning of infection, not only to prevent virulence gene induction, but also playing an active role in the adaptation of the bacterium to the epiphytic habitat. Comparison of the patterns of gene expression inside leaf tissues and during early colonization of leaf surfaces in the wild-type bacterium revealed 637 genes modulated between these two environments. More than 40% of these modulated genes are part of the PecS regulon, emphasizing the prominent role of PecS during plant colonization.
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Project description:Primary outcome(s): The exacerbation factors for PECS after colorectal ESD
| 2653581 | ecrin-mdr-crc
Project description:We investigated the covS-regulation of S. pyogenes in a hypervirulent M23 strain using RNA-sequencing. The differential gene expression comparison between the covS- mutant and isogenic wild type covS+ identified altered expression of 349 (18%) genes, including a broad spectrum of virulence genes and diverse metabolic genes. The data showed that the strain achieved hypervirulence by enhancing the expression of genes responsible for invasiveness and antiphagocytosis (i.e., hasABC), by abrogating the expression of toxic genes (i.e., speB), and by compromising gene products with dispensable functions (i.e., sfb1). Meanwhile, we found that covS also regulated diverse kinds of metabolic genes that maximized nutrient utilization and energy metabolism during growth and dissemination. From constructing a genome-scale metabolic model, we identified fourteen non-redundant metabolic gene modules, which constitute unique sources for specific nutrients. These genes were probably essential for pathogen growth and virulence. In general, this study provided quantitative transcriptomic signatures of the covS regulation in a hypervirulent S. pyogenes strain and addressed major aspects of the covS-modulated virulent mechanisms. Examination of expression profiling of covS- mutant strain and isogenic wild type covS+ at different growth stages.
2015-08-05 | E-GEOD-67533 | biostudies-arrayexpress
Project description:Transcriptome analysis of LPS stimulated PECs (WT and Zc3h12a S513A)
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Project description:The emergence of hypervirulent Klebsiella pneumoniae (hvKP) strains poses a significant threat to public health due to their high mortality rates and propensity to cause severe community-acquired infections in otherwise healthy individuals. The ability of hvKP to form biofilms and produce a protective capsule contributes to its enhanced virulence and is a significant challenge to effective antibiotic treatment. Therefore, understanding the molecular mechanisms underlying hvKP virulence and biofilm formation is crucial for developing new therapeutic strategies. Polyphosphate Kinase 1 (PPK1) is an enzyme responsible for inorganic polyphosphate synthesis and plays a vital role in regulating various physiological processes in bacteria. In this study, we investigated the impact of polyP metabolism on the biofilm and capsule formation and virulence traits in hvKP using Dictyostelium discoideum amoeba as a model host. We found that the PPK1 null-mutant was impaired in biofilm and capsule formation and showed attenuated virulence in D. discoideum compared to the wild-type strain. We performed a shotgun proteomic analysis of the PPK1 mutant and wild-type strain to gain further insight into the underlying molecular mechanism. The results revealed that the PPK1 mutant had a differential expression of proteins (DEP) involved in capsule synthesis (Wzi - Ugd), biofilm formation (MrkC-D-H), synthesis of the colibactin genotoxin precursor (ClbB), as well as proteins associated with the synthesis and modification of lipid A (ArnB -LpxC - PagP). These proteomic findings corroborate the phenotypic observations and indicate that the PPK1 mutation is associated with impaired biofilm and capsule formation and attenuated virulence in hypervirulent K. pneumoniae. Overall, our study highlights the importance of polyP synthesis in regulating extracellular biomolecules and virulence in K. pneumoniae and provides insights into potential therapeutic targets for treating K. pneumoniae infections.
2024-08-23 | PXD046644 | Pride