ArticleInfection and immunity2006
The GTPase Rab4 interacts with Chlamydia trachomatis inclusion membrane protein CT229.
Article in Infection and immunity, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.
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100 citing papers in PubMed, 149 citations in OpenAlex.
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- Transmembrane effector substrates of type IV secretion systems: mechanisms of secretion and insertion into host cell membranes.microLife · 2026Review
- CpoS-Inc interactions facilitate host cell modulation duringInfection and immunity · 2025Article
- Pathogenicity and virulence ofVirulence · 2025Review
- Genome-wide identification of modulators of Chlamydia trachomatis parasitophorous vacuole stability highlights an important role for sphingolipid supply.PLoS biology · 2025Article
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- Inc/GFP chimera protein-based interactomics reveals host cellular interactions of Cps0558, a novel Chlamydia psittaci inclusion protein.Pathogens and disease · 2025Article
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- Immunity to Sexually Transmitted Bacterial Infections of the Female Genital Tract: Toward Effective Vaccines.Vaccines · 2024Review
- ThemBio · 2023Article
- The emerging complexity of Chlamydia trachomatis interactions with host cells as revealed by molecular genetic approaches.Current opinion in microbiology · 2023Review
- Transmembrane substrates of type three secretion system injectisomes.Microbiology (Reading, England) · 2023Review
- Molecular pathogenesis ofFrontiers in cellular and infection microbiology · 2023Review
- Establishing the intracellular niche of obligate intracellular vacuolar pathogens.Frontiers in cellular and infection microbiology · 2023Review
- Chlamydia trachomatis Alters Mitochondrial Protein Composition and Secretes Effector Proteins That Target Mitochondria.mSphere · 2022Article
- The Chlamydia trachomatis inclusion membrane protein CT006 associates with lipid droplets in eukaryotic cells.PloS one · 2022Article
- Persistence Alters the Interaction between Chlamydia trachomatis and Its Host Cell.Infection and immunity · 2021Article
- Got mutants? How advances in chlamydial genetics have furthered the study of effector proteins.Pathogens and disease · 2021Review
- Akt Phosphorylation Influences Persistent Chlamydial Infection andFrontiers in cellular and infection microbiology · 2021Article
40 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Chlamydiae, which are obligate intracellular bacteria, replicate in a nonlysosomal vacuole, termed an inclusion. Although neither the host nor the chlamydial proteins that mediate the intracellular trafficking of the inclusion have been clearly identified, several enhanced green fluorescent protein (GFP)-tagged Rab GTPases, including Rab4A, are recruited to chlamydial inclusions. GFP-Rab4A associates with inclusions in a species-independent fashion by 2 h postinfection by mechanisms that have not yet been elucidated. To test whether chlamydial inclusion membrane proteins (Incs) recruit Rab4 to the inclusion, we screened a collection of chlamydial Incs for their ability to interact with Rab4A by using a yeast two-hybrid assay. From our analysis, we identified a specific interaction between Rab4A and Chlamydia trachomatis Inc CT229, which is expressed during the initial stages of infection. CT229 interacts with only wild-type Rab4A and the constitutively active GTPase-deficient Rab4AQ67L but not with the dominant-negative GDP-restricted Rab4AS22N mutant. To confirm the interaction between CT229 and Rab4A, we demonstrated that DsRed-CT229 colocalized with GFP-Rab4A in HeLa cells and more importantly wild-type and constitutively active GFP-Rab4A colocalized with CT229 at the inclusion membrane in C. trachomatis serovar L2-infected HeLa cells. Taken together, these data suggest that CT229 interacts with and recruits Rab4A to the inclusion membrane and therefore may play a role in regulating the intracellular trafficking or fusogenicity of the chlamydial inclusion.
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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.