ArticlePLoS pathogens2018
Chlamydia trachomatis inclusion membrane protein MrcA interacts with the inositol 1,4,5-trisphosphate receptor type 3 (ITPR3) to regulate extrusion formation.
Article in PLoS pathogens, 2018. 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
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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.
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Who cites it
46 citing papers in PubMed, 70 citations in OpenAlex.
- Live Imaging of Ions in Cells Infected with Chlamydia trachomatis.Methods in molecular biology (Clifton, N.J.) · 2027Article
- Genome-wide association studies ofInfection and immunity · 2026Article
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- Inclusion Membrane Proteins ofMicroorganisms · 2026Review
- Comparative transcriptomics reveals genes commonly induced by distinct stressors inInfection and immunity · 2026Article
- Comparative Transcriptomics Reveals Genes Commonly Induced by Distinct Stressors inbioRxiv : the preprint server for biology · 2025Article
- Pathogenicity and virulence ofVirulence · 2025Review
- Endoplasmic reticulum: the target of chlamydial manipulation.Archives of microbiology · 2025Review
- Recruitment of the cellular lipid transport protein CERT to C. psittaci inclusions regulates the timing of bacterial egress.Scientific reports · 2025Article
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- The acetylase activity of Cdu1 regulates bacterial exit from infected cells by protectingeLife · 2024Article
- Type 3 IP3 receptor: Its structure, functions, and related disease implications.Channels (Austin, Tex.) · 2023Review
- ThemBio · 2023Article
- The Fish Pathogen "Candidatus Clavichlamydia salmonicola"-A Missing Link in the Evolution of Chlamydial Pathogens of Humans.Genome biology and evolution · 2023Article
- Whole Genome Sequencing and Comparative Genomic Analysis ofPathogens (Basel, Switzerland) · 2023Article
- Article
- The Chlamydia trachomatis IncM Protein Interferes with Host Cell Cytokinesis, Centrosome Positioning, and Golgi Distribution and Contributes to the Stability of the Pathogen-Containing Vacuole.Infection and immunity · 2023Article
- Establishing the intracellular niche of obligate intracellular vacuolar pathogens.Frontiers in cellular and infection microbiology · 2023Review
- Molecular pathogenesis ofFrontiers in cellular and infection microbiology · 2023Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Chlamydia trachomatis is an obligate intracellular bacterium that replicates within a vacuole termed an inclusion. At the end of their intracellular developmental cycle, chlamydiae are released either by lysis of the host cell or extrusion of the intact inclusion. The inclusion membrane is extensively modified by the insertion of type III secreted inclusion membrane proteins, Incs, which contribute to inclusion membrane structure and facilitate host-pathogen interactions. An interaction was identified between the inclusion membrane protein, MrcA, and the Ca2+ channel inositol-1,4,5-trisphosphate receptor, type 3 (ITPR3). ITPR3 was recruited and localized to active Src-family-kinase rich microdomains on the inclusion membrane as was the Ca2+ sensor, STIM1. Disruption of MrcA by directed mutagenesis resulted in loss of ITPR3 recruitment and simultaneous reduction of chlamydial release by extrusion. Complementation of MrcA restored ITPR3 recruitment and extrusion. Inhibition of extrusion was also observed following siRNA depletion of host ITPR3 or STIM1. Chlamydial extrusion was also inhibited by the calcium chelator BAPTA-AM. Each of these treatments resulted in a concomitant reduction in phosphorylation of the myosin regulatory light chain (MLC2) and a loss of myosin motor activity at the end of the developmental cycle which is consistent with the reduced extrusion formation. These studies suggest that Ca2+ signaling pathways play an important role in regulation of release mechanisms by C. trachomatis.
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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.