YmoA functions as a molecular stress sensor in Yersinia
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ABSTRACT:
PROVIDER: PRJNA1177866 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31118983_1.fastq.gz | Fastqsanger.gz | |||
| SRR31118983_2.fastq.gz | Fastqsanger.gz | |||
| SRR31118984_1.fastq.gz | Fastqsanger.gz | |||
| SRR31118984_2.fastq.gz | Fastqsanger.gz | |||
| SRR31118985_1.fastq.gz | Fastqsanger.gz |
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Project description:Pathogenic bacteria sense and respond to environmental fluctuations, a capability essential for establishing successful infections. The YmoA/Hha protein family are conserved transcription regulators in Enterobacteriaceae, playing a critical role in these responses. Specifically, YmoA in Yersinia adjusts the expression of virulence-associated traits upon temperature shift. Still, the molecular mechanisms transducing environmental signals through YmoA remain elusive. Our study employed nuclear magnetic resonance spectroscopy, biological assays and RNA-seq analysis to elucidate these mechanisms. We demonstrated that YmoA underwent structural fluctuations and conformational dynamics in response to temperature and osmolarity changes, correlating with changes in plasmid copy number, bacterial fitness and virulence function. Notably, chemical shift analysis identified key roles of a few specific residues and of the C-terminus region in sensing both temperature and salt-driven switch. These findings demonstrate that YmoA acts as a central stress sensor in Yersinia, fine-tuning virulence gene expression and balancing metabolic trade-offs.
2024-10-28 | GSE280333 | GEO
Project description:Pathogenic bacteria sense and respond to environmental fluctuations, a capability essential for establishing successful infections. The YmoA/Hha protein family are conserved transcription regulators in Enterobacteriaceae, playing a critical role in these responses. Specifically, YmoA in Yersinia adjusts the expression of virulence-associated traits upon temperature shift. Still, the molecular mechanisms transducing environmental signals through YmoA remain elusive. Our study employs nuclear magnetic resonance spectroscopy, biological assays and RNA-seq analysis to elucidate these mechanisms. We demonstrate that YmoA undergoes structural fluctuations and conformational dynamics in response to temperature and osmolarity changes, correlating with changes in plasmid copy number, bacterial fitness and virulence function. Notably, chemical shift analysis identifies key roles of a few specific residues and of the C-terminus region in sensing both temperature and salt-driven switch. These findings demonstrate that YmoA acts as a central stress sensor in Yersinia, fine-tuning virulence gene expression and balancing metabolic trade-offs.
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Project description:Molecular surveillance of Yersinia enterocolitica
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Project description:Genome-wide alterations of gene expression were characterized using leukocytes collected from (informed and consented, all male) U.S. Army Ranger cadets immediately before and after training followed by exposure to a representative group of pathogens Yersinia pestis, dengue virus, Staphylococcus enterotoxin B. We employed experimental and computational approaches in identifying altered molecules, processes, pathways, and functional and regulatory networks mediating the host’s response towards battlefield-like stress, in assessing protective immunity status of the stressed host towards infection, and in identifying pathogen-induced biomarkers under severe stress background. We observed predicted inhibition of pathways significantly associated with lymphopoiesis, wound healing, inflammatory response, lymphocyte activation, apoptosis, and predicted activation of oxidative stress. Using weighted correlation network analyses, we showed preservation of these pathways across infection plus stress combinations. Regulatory networks comprising a common set of upstream regulators: transcription factors, microRNAs and post-translational regulators (kinases, phosphatases) may be drivers of molecular alterations leading compromised protective immunity. Other sets of transcripts were persistently altered in both the pre- and post-stress conditions due to the host’s response to each pathogen forming pathogen-specific molecular signatures with a potential to distinguish infection from that of severe stress. Our results suggest that severe battlefield-like stress alters molecular players implicated in the developments of hematopoietic stem cells probably leading to depletion of cellular and molecular repertoires of protective immunity, membrane trafficking of recycling endosomes and membrane translocation of the antigen processing mechanisms leading to suboptimal antigen processing and presentation, cell adhesion leading to impaired formation of productive immunological synapse, and inhibited T-cell activation. These factors may collectively be responsible for compromised protective immunity (infection susceptibility, delayed wound healing and poor vaccine response), and cellular anergy.
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Project description:Background: Severe stress can have drastic and systemic effects with dire implications on the health and wellbeing of exposed individuals. Particularly, the effect of stress on the immune response to infection is of interest because of its implications for vaccine efficacy and treatment strategy during stressful scenarios. Battlefield-like stress has previously been shown to cause an anergic state in the immune system that persists following exposure to a potent mitogen. Methods: Genome-wide alterations of gene expression were characterized using leukocytes collected from (15 informed and consented, all male) U.S. Army Ranger cadets immediately before and after training followed by exposure to a representative group of pathogens Yersinia pestis, dengue virus, Staphylococcus enterotoxin B (SEB). We employed experimental and computational approaches in identifying altered molecules, processes, pathways, and functional and regulatory networks mediating the host’s response towards battlefield-like stress, in assessing protective immunity status of the stressed host towards infection, and in identifying pathogen-induced biomarkers under severe stress background. Results: We observed predicted inhibition of pathways significantly associated with lymphopoiesis, wound healing, inflammatory response, lymphocyte activation, apoptosis, and predicted activation of oxidative stress. Using weighted correlation network analyses, we showed preservation of these pathways across infection plus stress combinations. Regulatory networks comprising a common set of upstream regulators: transcription factors, microRNAs and post-translational regulators (kinases, phosphatases) may be drivers of molecular alterations leading compromised protective immunity. Other sets of transcripts were persistently altered in both the pre- and post-stress conditions due to the host’s response to each pathogen forming pathogen-specific molecular signatures with a potential to distinguish infection from that of severe stress. Conclusion: Our results suggest that severe battlefield-like stress alters molecular players implicated in the developments of hematopoietic stem cells probably leading to depletion of cellular and molecular repertoires of protective immunity, membrane trafficking of recycling endosomes and membrane translocation of the antigen processing mechanisms leading to suboptimal antigen processing and presentation, cell adhesion leading to impaired formation of productive immunological synapse, and inhibited T-cell activation. These factors may collectively be responsible for compromised protective immunity (infection susceptibility, delayed wound healing and poor vaccine response), and cellular anergy.
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