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TRNA epitranscriptome determines pathogenicity of the opportunistic pathogen Pseudomonas aeruginosa

ABSTRACT: tRNA epitranscriptome determines pathogenicity of the opportunistic pathogen Pseudomonas aeruginosa

PROVIDER: PRJEB69610 | ENA |

REPOSITORIES: ENA

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tRNA epitranscriptome determines pathogenicity of the opportunistic pathogen Pseudomonas aeruginosa

Project description:tRNA epitranscriptome determines pathogenicity of the opportunistic pathogen Pseudomonas aeruginosa

| PRJNA627930 | ENA

RNA-Seq analysis for the study "tRNA epitranscriptome determines pathogenicity of the opportunistic pathogen Pseudomonas aeruginosa"

Project description:RNA-Seq analysis for the study "tRNA epitranscriptome determines pathogenicity of the opportunistic pathogen Pseudomonas aeruginosa"

| PRJNA627933 | ENA

tRNA epitranscriptome determines pathogenicity of the opportunistic pathogen <i>Pseudomonas aeruginosa</i>.

Project description:The success of bacterial pathogens depends on the coordinated expression of virulence determinants. Regulatory circuits that drive pathogenesis are complex, multilayered, and incompletely understood. Here, we reveal that alterations in tRNA modifications define pathogenic phenotypes in the opportunistic pathogen Pseudomonas aeruginosa. We demonstrate that the enzymatic activity of GidA leads to the introduction of a carboxymethylaminomethyl modification in selected tRNAs. Modifications at the wobble uridine base (cmnm5U34) of the anticodon drives translation of transcripts containing rare codons. Specifically, in P. aeruginosa the presence of GidA-dependent tRNA modifications modulates expression of genes encoding virulence regulators, leading to a cellular proteomic shift toward pathogenic and well-adapted physiological states. Our approach of profiling the consequences of chemical tRNA modifications is general in concept. It provides a paradigm of how environmentally driven tRNA modifications govern gene expression programs and regulate phenotypic outcomes responsible for bacterial adaption to challenging habitats prevailing in the host niche.

| S-EPMC10945773 | biostudies-literature

RNA-Seq and Ribo-Seq analyses of the study "tRNA epitranscriptome determines pathogenicity of the opportunistic pathogen Pseudomonas aeruginosa"

Project description:RNA-Seq and Ribo-Seq analyses of the study "tRNA epitranscriptome determines pathogenicity of the opportunistic pathogen Pseudomonas aeruginosa"

| PRJNA975827 | ENA

RNA-Seq analysis for the study "tRNA epitranscriptome determines pathogenicity of the opportunistic pathogen Pseudomonas aeruginosa"

2024-02-18 | GSE149304 | GEO

tRNA epitranscriptome determines pathogenicity of the opportunistic pathogen Pseudomonas aeruginosa

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-02-17 | GSE149306 | GEO

RNA-Seq and Ribo-Seq analyses of the study "tRNA epitranscriptome determines pathogenicity of the opportunistic pathogen Pseudomonas aeruginosa"

2024-02-18 | GSE233297 | GEO

Arsenic toxicity is regulated by queuine availability and oxidation-induced reprogramming of the human tRNA epitranscriptome

Project description:Cells respond to environmental stress by regulating gene expression at the level of both transcription and translation. The ~50 modified ribonucleotides of the human epitranscriptome contribute to the latter, with mounting evidence that dynamic regulation of tRNA wobble modifications leads to selective translation of stress response proteins from codon-biased genes. Here we show that the response of human HepG2 cells to arsenite exposure is regulated by the availability of queuine, a micronutrient and essential precursor to the wobble modification queuosine (Q) on tRNAs reading GUN codons. Among oxidizing and alkylating agents at equitoxic concentrations, arsenite exposure caused an oxidant-specific increase in Q that correlated with up-regulation of proteins from codon-biased genes involved in energy metabolism. Limiting queuine increased arsenite-induced cell death, altered translation, increased reactive oxygen species levels, and caused mitochondrial dysfunction. In addition to revealing a new epitranscriptomic facet of arsenite toxicity and response, our results highlight the mechanistic links between environmental exposures, stress tolerance, and micronutrients.

2022-08-27 | PXD030726 | Pride

Arsenic toxicity is regulated by queuine availability and oxidation- induced reprogramming of the human tRNA epitranscriptome

2022-06-03 | GSE205332 | GEO

Lack of TRMT2A, a tRNA methyltransferase, induces the generation of tRNA-derived small RNAs due to m5U54 tRNA hypomodification [Array]

Project description:Transfer RNA (tRNA) molecules contain a variety of post-transcriptional modifications which are crucial for tRNA stability, translation efficiency, and fidelity. Besides their canonical roles in translation, tRNAs also originate tRNA-derived small RNAs (tsRNAs), a class of small non-coding RNAs with regulatory functions ranging from translation regulation, to gene expression control and cellular stress response. Recent evidence show that tsRNAs are also modified, however the impact of tRNA epitranscriptome deregulation on tsRNAs generation is only now beginning to be uncovered. The 5-methyluridine (m5U) modification at position 54 of cytosolic tRNAs is one of the most common and conserved tRNA modifications among species. This modification is catalyzed by the tRNA methyltransferase TRMT2A, but its biological role remains largely unexplored. Here, we show that TRMT2A knockdown in human cells induces m5U54 tRNA hypomodification, resulting in angiogenin (ANG) dependent tsRNA formation. More specifically, m5U54 hypomodification is followed by ANG overexpression and tRNA cleavage near the anticodon, resulting in accumulation of 5’tRNA-derived stress-induced RNAs (5’tiRNAs), in particular 5’tiRNA-GlyGCC and 5’tiRNA-GluCTC. Additionally, transcriptomic analysis confirms that down-regulation of TRMT2A and consequently m5U54 hypomodification impacts the cellular stress response and RNA stability, which is often correlated with tsRNA generation. Accordingly, exposure to oxidative stress conditions induces TRMT2A down-regulation and tsRNA formation in mammalian cells. These results establish a link between tRNA demethylation and tsRNAs formation and unravel m5U54 as a tRNA cleavage protective mark.

2021-04-20 | GSE164168 | GEO

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