ArticleCellular microbiology2009
Targeting eEF1A by a Legionella pneumophila effector leads to inhibition of protein synthesis and induction of host stress response.
Article in Cellular microbiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
94 citing papers in PubMed, 145 citations in OpenAlex.
- Crystal structure of Legionella pneumophila glycosidase effector LegY.Acta crystallographica. Section F, Structural biology communications · 2026Article
- Article
- Legionella effector protein SidG disrupts host cytoskeleton via targeting Arp2/3 complex.PLoS pathogens · 2026Article
- Article
- Article
- GM-CSF engages multiple signaling pathways to enhance pro-inflammatory cytokine responses in human monocytes duringInfection and immunity · 2025Article
- ThemSphere · 2025Article
- Review
- A comprehensive two-hybrid analysis to explore themSystems · 2024Article
- A random mutagenesis screen enriched for missense mutations in bacterial effector proteins.G3 (Bethesda, Md.) · 2024Article
- Bacterial ubiquitin ligases hijack the host deubiquitinase OTUB1 to inhibit MTORC1 signaling and promote autophagy.Autophagy · 2024Article
- A pyocin-like T6SS effector mediates bacterial competition inMicrobiology spectrum · 2024Article
- Insights into the role of legionella effectors on host metabolic perturbations.Frontiers in cellular and infection microbiology · 2024Review
- Article
- A Legionella toxin exhibits tRNA mimicry and glycosyl transferase activity to target the translation machinery and trigger a ribotoxic stress response.Nature cell biology · 2023Article
- Hijacking host ribosomes via tRNA mimicry.Nature cell biology · 2023Article
- Eat or Be Eaten: Strategies Used byInfection and immunity · 2023Review
- Intrabacterial Regulation of a Cytotoxic Effector by Its Cognate Metaeffector Promotes Legionella pneumophila Virulence.mSphere · 2023Article
- H3-T6SS of Pseudomonas aeruginosa PA14 contributes to environmental adaptation via secretion of a biofilm-promoting effector.Stress biology · 2022Article
- Concept about the Virulence Factor ofMicroorganisms · 2022Review
34 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The Legionella pneumophila Dot/Icm type IV secretion system is essential for the biogenesis of a phagosome that supports bacterial multiplication, most likely via the functions of its protein substrates. Recent studies indicate that fundamental cellular processes, such as vesicle trafficking, stress response, autophagy and cell death, are modulated by these effectors. However, how each translocated protein contributes to the modulation of these pathways is largely unknown. In a screen to search substrates of the Dot/Icm transporter that can cause host cell death, we identified a gene whose product is lethal to yeast and mammalian cells. We demonstrate that this protein, called SidI, is a substrate of the Dot/Icm type IV protein transporter that targets the host protein translation process. Our results indicate that SidI specifically interacts with eEF1A and eEF1Bgamma, two components of the eukaryotic protein translation elongation machinery and such interactions leads to inhibition of host protein synthesis. Furthermore, we have isolated two SidI substitution mutants that retain the target binding activity but have lost toxicity to eukaryotic cells, suggesting potential biochemical effect of SidI on eEF1A and eEF1Bgamma. We also show that infection by L. pneumophila leads to eEF1A-mediated activation of the heat shock regulatory protein HSF1 in a virulence-dependent manner and deletion of sidI affects such activation. Moreover, similar response occurred in cells transiently transfected to express SidI. Thus, inhibition of host protein synthesis by specific effectors contributes to the induction of stress response in L. pneumophila-infected cells.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.