ArticleJournal of bacteriology2016
A Functional Core of IncA Is Required for Chlamydia trachomatis Inclusion Fusion.
Article in Journal of bacteriology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed, 62 citations in OpenAlex.
- Live Cell Imaging of Chlamydia Inclusion Membrane Proteins Using Genetically Encoded Antibodies.Methods in molecular biology (Clifton, N.J.) · 2027Article
- A Conditional Knockout Mutant Approach to Study Essential Genes in Chlamydia in Cell Culture and In Vivo.Methods in molecular biology (Clifton, N.J.) · 2027Article
- Inclusion Membrane Proteins ofMicroorganisms · 2026Review
- ThemBio · 2026Article
- Minute-scale control of ubiquitin-mediated degradation reveals dynamics of bacterial secreted effector-functions.Nature communications · 2026Article
- Adaptive metabolic strategies of intracellular bacterial pathogens.Frontiers in microbiology · 2026Review
- CpoS-Inc interactions facilitate host cell modulation duringInfection and immunity · 2025Article
- Pathogenicity and virulence ofVirulence · 2025Review
- ThebioRxiv : the preprint server for biology · 2025Article
- Article
- The Chlamydia effector Dre1 binds dynactin to reposition host organelles during infection.Cell reports · 2025Article
- Article
- Hijacking host cell vesicular transport: New insights into the nutrient acquisition mechanism ofVirulence · 2024Review
- Specialized contact sites regulate the fusion of chlamydial inclusion membranes.Nature communications · 2024Article
- The Chlamydia effector IncE employs two short linear motifs to reprogram host vesicle trafficking.Cell reports · 2024Article
- Genomic insights into local-scale evolution of ocularMicrobial genomics · 2024Article
- Zoonotic and other veterinary chlamydiae - an update, the role of the plasmid and plasmid-mediated transformation.Pathogens and disease · 2024Review
- Intracellular lifestyle of Chlamydia trachomatis and host-pathogen interactions.Nature reviews. Microbiology · 2023Review
- Molecular pathogenesis ofFrontiers in cellular and infection microbiology · 2023Review
- Transmembrane substrates of type three secretion system injectisomes.Microbiology (Reading, England) · 2023Review
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
unlabelledChlamydia trachomatis is an obligate intracellular pathogen that is the etiological agent of a variety of human diseases, including blinding trachoma and sexually transmitted infections. Chlamydiae replicate within a membrane-bound compartment, termed an inclusion, which they extensively modify by the insertion of type III secreted proteins called Inc proteins. IncA is an inclusion membrane protein that encodes two coiled-coil domains that are homologous to eukaryotic SNARE (soluble N-ethylmaleimide-sensitive factor attachment receptor) motifs. Recent biochemical evidence suggests that a functional core, composed of SNARE-like domain 1 (SLD-1) and part of SNARE-like domain 2 (SLD-2), is required for the characteristic homotypic fusion of C. trachomatis inclusions in multiply infected cells. To verify the importance of IncA in homotypic fusion in Chlamydia, we generated an incA::bla mutant. Insertional inactivation of incA resulted in the formation of nonfusogenic inclusions, a phenotype that was completely rescued by complementation with full-length IncA. Rescue of homotypic inclusion fusion was dependent on the presence of the functional core consisting of SLD-1 and part of SLD-2. Collectively, these results confirm in vitro membrane fusion assays identifying functional domains of IncA and expand the genetic tools available for identification of chlamydia with a method for complementation of site-specific mutants. IMPORTANCE: Chlamydia trachomatis replicates within a parasitophorous vacuole termed an inclusion. The chlamydial inclusions are nonfusogenic with vesicles in the endocytic pathway but, in multiply infected cells, fuse with each other to form a single large inclusion. This homotypic fusion is dependent upon the presence of a chlamydial inclusion membrane-localized protein, IncA. Specificity of membrane fusion in eukaryotic cells is regulated by SNARE (soluble N-ethylmaleimide sensitive factor attachment receptor) proteins on the cytosolic face of vesicles and target membranes. IncA contains two SNARE-like domains. Newly developed genetic tools for the complementation of targeted mutants in C. trachomatis are used to confirm the minimal requirement of SNARE-like motifs necessary to promote the homotypic fusion of inclusions.
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.