ArticleNucleic acids research2019
Optimal translational fidelity is critical for Salmonella virulence and host interactions.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 32 citations in OpenAlex.
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- Deficiency in ribosome biogenesis causes streptomycin resistance and impairs motility inbioRxiv : the preprint server for biology · 2024Article
- Colonization of larval zebrafish (mSphere · 2023Article
- Global profiling of ribosomal protein acetylation reveals essentiality of acetylation homeostasis in maintaining ribosome assembly and function.Nucleic acids research · 2023Article
- Genome-wide screening reveals metabolic regulation of stop-codon readthrough by cyclic AMP.Nucleic acids research · 2023Article
- BBQ methods: Streamlined workflows for Bacterial Burden Quantification in infected cells by confocal microscopy.bioRxiv : the preprint server for biology · 2023Article
- Zebrafish-based platform for emerging bio-contaminants and virus inactivation research.The Science of the total environment · 2023Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Translational fidelity is required for accurate flow of genetic information, but is frequently altered by genetic changes and environmental stresses. To date, little is known about how translational fidelity affects the virulence and host interactions of bacterial pathogens. Here we show that surprisingly, either decreasing or increasing translational fidelity impairs the interactions of the enteric pathogen Salmonella Typhimurium with host cells and its fitness in zebrafish. Host interactions are mediated by Salmonella pathogenicity island 1 (SPI-1). Our RNA sequencing and quantitative RT-PCR results demonstrate that SPI-1 genes are among the most down-regulated when translational fidelity is either increased or decreased. Further, this down-regulation of SPI-1 genes depends on the master regulator HilD, and altering translational fidelity destabilizes HilD protein via enhanced degradation by Lon protease. Our work thus reveals that optimal translational fidelity is pivotal for adaptation of Salmonella to the host environment, and provides important mechanistic insights into this process.
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