Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1218897 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32254900_1.fastq.gz | Fastqsanger.gz | |||
| SRR32254900_2.fastq.gz | Fastqsanger.gz | |||
| SRR32254894_1.fastq.gz | Fastqsanger.gz | |||
| SRR32254894_2.fastq.gz | Fastqsanger.gz | |||
| SRR32254895_1.fastq.gz | Fastqsanger.gz |
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Project description:To better understand the role of H. ducreyi CpxRA in controlling virulence determinants, here we defined genes potentially regulated by CpxRA by using RNA-Seq. Activation of CpxR by deletion of cpxA repressed nearly 70% of its targets, including seven established virulence determinants. Inactivation of CpxR by deletion of cpxR differentially regulated few genes and increased the expression of one virulence determinant. We identified a CpxR binding motif that was enriched in downregulated but not upregulated targets. These data reinforce the hypothesis that CpxA phosphatase activity plays a critical role in controlling H. ducreyi virulence in vivo. Characterization of the downregulated genes may offer new insights into pathogenesis. RNA of Haemophilus ducreyi wildtype, cpxA and cpxR mutants were collected at mid-log, transition, and stationary phases of growth, in quadruplicate.
2015-11-21 | E-GEOD-75237 | biostudies-arrayexpress
Project description:To better understand the role of H. ducreyi CpxRA in controlling virulence determinants, here we defined genes potentially regulated by CpxRA by using RNA-Seq. Activation of CpxR by deletion of cpxA repressed nearly 70% of its targets, including seven established virulence determinants. Inactivation of CpxR by deletion of cpxR differentially regulated few genes and increased the expression of one virulence determinant. We identified a CpxR binding motif that was enriched in downregulated but not upregulated targets. These data reinforce the hypothesis that CpxA phosphatase activity plays a critical role in controlling H. ducreyi virulence in vivo. Characterization of the downregulated genes may offer new insights into pathogenesis.
2015-11-21 | GSE75237 | GEO
Project description:To better understand the role of Neisseria gonorrhoeae CpxRA in controlling virulence determinants, here we defined genes potentially regulated by CpxRA by using RNA-Seq. We identified approximately 139 genes differentially expressed between cpxA (Cpx system active) and cpxR (Cpx system inactive) mutants. A large number of the differentially expressed genes encode envelope-localized proteins.
2016-09-01 | GSE83341 | GEO
Project description:The type III secretion system (T3SS) is a cell envelope-spanning injectisome found in many Gram negative pathogens. Expression of the T3SS is controlled by extracellular signals such as cell envelope stress. For example, the CpxAR two component system negatively regulates the Yersinia pseudotuberculosis Ysc T3SS, although the mechanism for this regulation remains unclear. As expected from previous studies, we found that mutations in Y. pseudotuberculosis that lock CpxR in its constitutively activated state (∆cpxA and cpxRD51E) led to decreased expression of the Ysc T3SS. CpxR did not bind to the regulatory regions of lcrF, encoding the Ysc T3SS master regulator. However, overexpression of LcrF protein rescued the T3SS expression defect of the ∆cpxA and cpxRD51E mutants, suggesting that CpxR represses lcrF through an indirect mechanism. Transcriptome analysis of Y. pseudotuberculosis showed that 101 genes were upregulated and 77 genes downregulated in both the ∆cpxA and cpxRD51E strains compared to wildtype, including seven genes known to modulate transcription. Individual deletion of these seven regulatory factors did not identify any single gene responsible for CpxR-dependent repression of LcrF, suggesting that the CpxAR system may act through multiple pathways to indirectly regulate the Ysc T3SS. However, this analysis led us to examine the role of the OmpR/EnvZ two component regulatory system, which is responsive to osmolarity, in LcrF regulation. Deletion of ompR led to a two-fold increase in LcrF and T3SS expression. These results suggest more complex regulation of the Ysc T3SS by two component regulatory systems than previously appreciated.
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Project description:The bacterium Legionella pneumophila is capable of intracellular replication within freshwater protozoa as well as human alveolar macrophages, the latter of which results in the serious pneumonia Legionnaires’ disease. A primary factor involved in these host cell interactions is the Dot/Icm Type IV secretion system that is responsible for translocating effector proteins needed to establish and maintain the bacterial replicative niche. Several regulatory factors have been identified to control the expression of the Dot/Icm system and effectors, one of which is the CpxRA two-component system, suggesting essentiality for virulence. However, studies elsewhere have shown that L. pneumophila strains harboring mutated cpxRA genes have minimal to no impact on L. pneumophila intracellular growth in protozoa and macrophages. In this study, we generated L. pneumophila cpxR, cpxA, and cpxRA in-frame null mutant strains to further delineate the role of the CpxRA system in bacterial survival and virulence. Surprisingly, we found that cpxR and cpxRA are essential for intracellular replication within Acanthamoeba castellanii, but not in U937 macrophage-like cells. Transcriptome analysis revealed that CpxRA regulates a large number of virulence-associated proteins including a number of Dot/Icm effectors as well as 14 Type II secreted substrates. Furthermore, the cpxR and cpxRA mutants were more sodium resistant than wildtype, and cpxRA expression reaches maximal levels during post-exponential phase. Taken together, our findings suggest the CpxRA system is a key contributor to L. pneumophila virulence via virulence factor regulation.
2016-09-16 | GSE73873 | GEO
Project description:Klebsiella pneumoniae is a prominent human pathogen that has developed resistance to multiple antibiotics. While the roles of capsules and siderophores are well established, the identification of additional virulence determinants remains limited. In this study, we hypothesize that the two-component system response regulator CpxR is integral to the regulation of K. pneumoniae virulence via control of specific virulence-associated genes. Deletion of the cpxR gene resulted in reduced serum resistance and attenuated virulence in both Galleria mellonella larvae and murine infection models compared to the wild-type strain. To elucidate the repertoire of virulence-associated genes regulated by CpxR, a multidisciplinary workflow was employed, integrating RNA sequencing, Real-Time quantitative PCR, gene knockout strategies, serum resistance assays, and infection experiments utilizing Galleria mellonella. Among the genes identified with significantly diminished expression following cpxR deletion, KPHS_28080 emerged as a novel candidate virulence-associated gene. Deletion of KPHS_28080 impaired serum survival in both the carbapenem-resistant CRKp HS11286 and the hypervirulent hvKp ATCC43816 strains. Furthermore, deletion of KPHS_28080 in hvKp ATCC43816 led to significantly decreased colonization and impaired dissemination to multiple organs in murine models, corresponding with an overall reduction in virulence. The promoter region of KPHS_28080 harbors a conserved CpxR binding motif, which enhances promoter activity and gene transcription upon CpxR binding. Sequence alignment revealed that KPHS_28080 encodes a member of the short-chain dehydrogenase family, and this gene is highly conserved among K. pneumoniae strains. These results elucidate the pivotal role of CpxR in mediating virulence in K. pneumoniae and clarify its regulatory impact on virulence-associated gene expression.
2025-07-10 | GSE300466 | GEO
Project description:Pathogenic bacteria export large proteins and protein complexes, including virulence factors, using dedicated trans-envelope multi-protein machineries, collectively called secretion systems. Four of these protein export machines found in Gram-negative bacteria: type 2 and 3 secretion systems, the type 4 pilus biogenesis system and the filamentous phage assembly-secretion system (FFSS), contain large homologous gated channels in the outer membrane, called secretins. These channels are radially symmetrical homomultimers (luminal diameter 6-8 nm) interrupted by an internal septum, which blocks the channel in its resting state. By analyzing the transcriptome of Escherichia coli producing the FFSS secretin pIV and an isogenic leaky-gate variant, we have expanded the known secretin responses to include the Sox, Cpx, Rcs and RyhB regulons, in addition to the known secretin responder, the Psp regulon. Furthermore, we show that responses dependent on transcriptional regulators CpxR, SoxS and RcsB (in addition to PspF) are required for survival of E. coli producing the leaky-gate variant of secretin pIV, while CpxR, SoxS and PspF are required for survival of cells producing wild-type T3SS secretin InvG. Our analysis shows that secretins induce three out of six envelope stress responses and responses to oxidative stress. Identification of the key stress response regulators required for survival of secretin stress suggests pathways that may be of interest in developing strategies for control of secretin-expressing pathogenic bacteria.
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Project description:A novel hybrid two-component system Lvr mediates virulence and global regulation in pathogenic Leptospira
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