The small protein YjiS acts as a virulence suppressor in Salmonella Typhimurium
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PROVIDER: PRJNA1075134 | ENA |
REPOSITORIES: ENA
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Project description:Bacterial small proteins impact diverse physiological processes, however, technical challenges posed by small size hampered their systematic identification and biochemical characterization. In our quest to uncover small proteins relevant for Salmonella pathogenicity, we previously identified YjiS, a 54 amino acid protein, which is strongly induced during this pathogen’s intracellular infection stage and exhibits features of a virulence suppressor. Here, we set out to further characterize the virulence-related role of YjiS. Cell culture infection assays with Salmonella mutants lacking or overexpressing YjiS corroborated previous functional genomics data and additionally suggested this small protein to counteract bacterial escape from macrophages. Mutant scanning of the protein’s conserved, arginine-rich DUF1127 domain excluded a major effect of single amino acid substitutions on the infection phenotype. A comparative dual RNA-seq assay uncovered the molecular footprint of YjiS in the macrophage response to infection, with effects related to oxidative stress and endo-/exocytosis. Bacterial cell fractionation experiments demonstrated YjiS to associate with the inner membrane, without being itself membrane-inserted. Accordingly, proteins interacting with YjiS in pull-down experiments were enriched for inner membrane processes. Together, our study points to a role for Salmonella YjiS as a membrane-associated suppressor of pathogen dissemination.
2025-01-15 | GSE255513 | GEO
Project description:Bacterial small proteins impact diverse physiological processes, however, technical challenges posed by small size hampered their systematic identification and biochemical characterization. In our quest to uncover small proteins relevant for Salmonella pathogenicity, we previously identified YjiS, a 54 amino acid protein, which is strongly induced during this pathogen’s intracellular infection stage and exhibits features of a virulence suppressor. Here, we set out to further characterize the virulence-related role of YjiS. Cell culture infection assays with Salmonella mutants lacking or overexpressing YjiS corroborated previous functional genomics data and additionally suggested this small protein to counteract bacterial escape from macrophages. Mutant scanning of the protein’s conserved, arginine-rich DUF1127 domain excluded a major effect of single amino acid substitutions on the infection phenotype. A comparative dual RNA-seq assay uncovered the molecular footprint of YjiS in the macrophage response to infection, with effects related to oxidative stress and endo-/exocytosis. Bacterial cell fractionation experiments demonstrated YjiS to associate with the inner membrane, without being itself membrane-inserted. Accordingly, proteins interacting with YjiS in pull-down experiments were enriched for inner membrane processes. Together, our study points to a role for Salmonella YjiS as a membrane-associated suppressor of pathogen dissemination.
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Project description:<p><em>Salmonella Typhimurium</em> establishes systemic infection by replicating in host macrophages. Here we show that macrophages infected with <em>S. Typhimurium</em> exhibit upregulated glycolysis and decreased serine synthesis, leading to accumulation of glycolytic intermediates. The effects on serine synthesis are mediated by bacterial protein SopE2, a type III secretion system (T3SS) effector encoded in pathogenicity island SPI-1. The changes in host metabolism promote intracellular replication of <em>S. Typhimurium</em> via two mechanisms: decreased glucose levels lead to upregulated bacterial uptake of 2- and 3-phosphoglycerate and phosphoenolpyruvate (carbon sources), while increased pyruvate and lactate levels induce upregulation of another pathogenicity island, SPI-2, known to encode virulence factors. Pharmacological or genetic inhibition of host glycolysis, activation of host serine synthesis, or deletion of either the bacterial transport or signal sensor systems for those host glycolytic intermediates impairs <em>S. Typhimurium</em> replication or virulence.</p>
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