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Evidence for a post-invasion role of the Chlamydia trachomatis type III secreted effector TmeA in redirection of host plasma membrane-derived material
Evidence for a post-invasion role of the Chlamydia trachomatis type III secreted effector TmeA in redirection of host plasma membrane-derived material
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Evidence for a post-invasion role of the Chlamydia trachomatis type III secreted effector TmeA in redirection of host plasma membrane-derived material
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Evidence for a post-invasion role of the Chlamydia trachomatis type III secreted effector TmeA in redirection of host plasma membrane-derived material
Evidence for a post-invasion role of the Chlamydia trachomatis type III secreted effector TmeA in redirection of host plasma membrane-derived material

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Evidence for a post-invasion role of the Chlamydia trachomatis type III secreted effector TmeA in redirection of host plasma membrane-derived material
Evidence for a post-invasion role of the Chlamydia trachomatis type III secreted effector TmeA in redirection of host plasma membrane-derived material
Journal Article

Evidence for a post-invasion role of the Chlamydia trachomatis type III secreted effector TmeA in redirection of host plasma membrane-derived material

2025
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Overview
Chlamydia trachomatis is a human pathogen and a prevalent agent of sexually transmitted diseases. The ability to survive and propagate within a protected intracellular niche leads directly to pathology indicative of Chlamydia -mediated disease. The reduced chlamydial genome leads to comparatively limited biosynthetic capacity, thereby necessitating parasitism of metabolites and other resources from the infected host cell. Chlamydia relies heavily on type III secreted effectors to interface with and co-opt host pathways to acquire resources. We demonstrate herein that the plasma membranes of infected cells represent a potential reservoir of resources required for optimal intracellular growth. Chlamydiae employ at least one type III secreted effector protein, translocated membrane-associated effector A (TmeA), to redirect material to the vacuole by manipulating Arp2/3-dependent actin polymerization. This pathway represents a distinct mechanism by which Chlamydia acquires resources and provides evidence for TmeA function during intracellular development.
Publisher
American Society for Microbiology,American Society for Microbiology (ASM)
Subject

Actin

/ Actins - metabolism

/ Adherent-Invasive E. coli Pathogenesis

/ Bacterial Internalization

/ Bacterial Proteins - genetics

/ Bacterial Proteins - metabolism

/ Bacteriology

/ Cell Membrane - metabolism

/ Cell Membrane - microbiology

/ Chlamydia

/ Chlamydia Infections - microbiology

/ Chlamydia trachomatis

/ Chlamydia trachomatis - genetics

/ Chlamydia trachomatis - metabolism

/ Chlamydia trachomatis - pathogenicity

/ Clathrin

/ Clinical Microbiology and Infectious Diseases

/ Cytoskeleton

/ Dynamin

/ Editor’s Pick

/ Gene expression

/ Genitourinary Infections

/ Genomes

/ HeLa Cells

/ Host Cell Invasion

/ Host Cell Manipulation

/ Host-Microbial Interactions

/ Host-Pathogen Interactions

/ Humans

/ Inclusion Bodies - metabolism

/ Inclusion Bodies - microbiology

/ Infections

/ Intracellular

/ Intracellular Pathogen Survival

/ Intracellular Survival

/ Intracellular Trafficking after Invasion

/ Invasion and Intracellular Survival

/ lipid

/ Lipids

/ Lipophilic

/ Mechanisms of Host Cell Invasion

/ Membrane trafficking

/ Microbial Pathogenesis and Immunology

/ N-WASP protein

/ obligate intracellular

/ Oral Pathogen Pathogenesis

/ Organelles

/ Parasitism

/ Pathogenesis

/ Pathogens

/ Plasma membranes

/ Polymerization

/ Protein Secretion Systems

/ Protein Transport

/ Proteins

/ Quality control

/ Research Article

/ Role in Virulence and Host Interaction

/ Sexually transmitted diseases

/ Sphingomyelin

/ STD

/ TmeA

/ Type III Secretion Systems - genetics

/ Type III Secretion Systems - metabolism

/ Vacuoles - microbiology

/ vesicle trafficking

/ Viral Gastroenteritis

/ Wiskott-Aldrich Syndrome Protein, Neuronal - metabolism