ArticleInfection and immunity2016
Tryptophan Codon-Dependent Transcription in Chlamydia pneumoniae during Gamma Interferon-Mediated Tryptophan Limitation.
Article in Infection and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- Circulating biomarkers of infection and endometrial cancer risk.Cancer causes & control : CCC · 2025Article
- Effect of tryptophan starvation on inclusion membrane composition and chlamydial-host interactions.Infection and immunity · 2025Article
- Metabolic model guided CRISPRi identifies a central role for phosphoglycerate mutase inmSystems · 2024Article
- Metabolism and physiology of pathogenic bacterial obligate intracellular parasites.Frontiers in cellular and infection microbiology · 2024Review
- Tryptophan Availability during Persistence of Chlamydia trachomatis Directly Impacts Expression of Chlamydial Cell Division Proteins.Infection and immunity · 2023Article
- Persistence of obligate intracellular pathogens: alternative strategies to overcome host-specific stresses.Frontiers in cellular and infection microbiology · 2023Review
- The role of infected epithelial cells inFrontiers in cellular and infection microbiology · 2023Review
- Host Cell Amplification of Nutritional Stress Contributes To Persistence in Chlamydia trachomatis.mBio · 2022Article
- Localized cardiolipin synthesis is required for the assembly of MreB during the polarized cell division of Chlamydia trachomatis.PLoS pathogens · 2022Article
- Incorporation of transition to transversion ratio and nonsense mutations, improves the estimation of the number of synonymous and non-synonymous sites in codons.DNA research : an international journal for rapid publication of reports on genes and genomes · 2022Article
- Article
- Persistence Alters the Interaction between Chlamydia trachomatis and Its Host Cell.Infection and immunity · 2021Article
- Genome copy number regulates inclusion expansion, septation, and infectious developmental form conversion inJournal of bacteriology · 2021Article
- The iron-dependent repressor YtgR is a tryptophan-dependent attenuator of the trpRBA operon in Chlamydia trachomatis.Nature communications · 2020Article
- Article
- Inhibition of tRNA Synthetases Induces Persistence inInfection and immunity · 2020Article
- Persistence of Intracellular Bacterial Pathogens-With a Focus on the Metabolic Perspective.Frontiers in cellular and infection microbiology · 2020Review
- Functional inhibition of acid sphingomyelinase disrupts infection by intracellular bacterial pathogens.Life science alliance · 2019Article
- Initial Characterization of the Two ClpP Paralogs ofJournal of bacteriology · 2019Article
- Diet-Related Metabolic Perturbations of Gut Microbial Shikimate Pathway-Tryptamine-tRNA Aminoacylation-Protein Synthesis in Human Health and Disease.International journal of tryptophan research : IJTR · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In evolving to an obligate intracellular niche, Chlamydia has streamlined its genome by eliminating superfluous genes as it relies on the host cell for a variety of nutritional needs like amino acids. However, Chlamydia can experience amino acid starvation when the human host cell in which the bacteria reside is exposed to interferon gamma (IFN-γ), which leads to a tryptophan (Trp)-limiting environment via induction of the enzyme indoleamine-2,3-dioxygenase (IDO). The stringent response is used to respond to amino acid starvation in most bacteria but is missing from Chlamydia Thus, how Chlamydia, a Trp auxotroph, responds to Trp starvation in the absence of a stringent response is an intriguing question. We previously observed that C. pneumoniae responds to this stress by globally increasing transcription while globally decreasing translation, an unusual response. Here, we sought to understand this and hypothesized that the Trp codon content of a given gene would determine its transcription level. We quantified transcripts from C. pneumoniae genes that were either rich or poor in Trp codons and found that Trp codon-rich transcripts were increased, whereas those that lacked Trp codons were unchanged or even decreased. There were exceptions, and these involved operons or large genes with multiple Trp codons: downstream transcripts were less abundant after Trp codon-rich sequences. These data suggest that ribosome stalling on Trp codons causes a negative polar effect on downstream sequences. Finally, reassessing previous C. pneumoniae microarray data based on codon content, we found that upregulated transcripts were enriched in Trp codons, thus supporting our hypothesis.
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Registered trials
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