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CteG is a Chlamydia trachomatis effector protein that associates with the Golgi complex of infected host cells

Chlamydia trachomatis is a bacterial pathogen causing ocular and genital infections in humans. C. trachomatis multiplies exclusively inside host cells within a characteristic vacuole, from where it manipulates host cells by injecting them with type III secretion effector proteins. Here, we identifie...

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Autores principales: Pais, Sara V., Key, Charlotte E., Borges, Vítor, Pereira, Inês S., Gomes, João Paulo, Fisher, Derek J., Mota, Luís Jaime
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6468002/
https://www.ncbi.nlm.nih.gov/pubmed/30992493
http://dx.doi.org/10.1038/s41598-019-42647-3
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author Pais, Sara V.
Key, Charlotte E.
Borges, Vítor
Pereira, Inês S.
Gomes, João Paulo
Fisher, Derek J.
Mota, Luís Jaime
author_facet Pais, Sara V.
Key, Charlotte E.
Borges, Vítor
Pereira, Inês S.
Gomes, João Paulo
Fisher, Derek J.
Mota, Luís Jaime
author_sort Pais, Sara V.
collection PubMed
description Chlamydia trachomatis is a bacterial pathogen causing ocular and genital infections in humans. C. trachomatis multiplies exclusively inside host cells within a characteristic vacuole, from where it manipulates host cells by injecting them with type III secretion effector proteins. Here, we identified CteG as the first C. trachomatis effector associated with the Golgi. For this, C. trachomatis strains expressing candidate effectors fused to a double hemagglutinin (2HA) tag were constructed. Then, among these strains, immunofluorescence microscopy revealed that CteG-2HA was delivered into the cytoplasm of infected cells. Between 16–20 h post-infection, CteG-2HA mostly associated with the Golgi; however, CteG-2HA also appeared at the host cell plasma membrane, and at 30 or 40 h post-infection this was its predominant localization. This change in the main localization of CteG-2HA was independent of intact microfilaments or microtubules. Ectopic expression of different regions of CteG (656 amino acid residues) in uninfected cells revealed that its first 100 residues contain a Golgi targeting region. Although a C. trachomatis cteG mutant did not display a defect in intracellular multiplication, CteG induced a vacuolar protein sorting defect when expressed in Saccharomyces cerevisiae. This suggested that CteG might function by subverting host cell vesicular transport.
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spelling pubmed-64680022019-04-23 CteG is a Chlamydia trachomatis effector protein that associates with the Golgi complex of infected host cells Pais, Sara V. Key, Charlotte E. Borges, Vítor Pereira, Inês S. Gomes, João Paulo Fisher, Derek J. Mota, Luís Jaime Sci Rep Article Chlamydia trachomatis is a bacterial pathogen causing ocular and genital infections in humans. C. trachomatis multiplies exclusively inside host cells within a characteristic vacuole, from where it manipulates host cells by injecting them with type III secretion effector proteins. Here, we identified CteG as the first C. trachomatis effector associated with the Golgi. For this, C. trachomatis strains expressing candidate effectors fused to a double hemagglutinin (2HA) tag were constructed. Then, among these strains, immunofluorescence microscopy revealed that CteG-2HA was delivered into the cytoplasm of infected cells. Between 16–20 h post-infection, CteG-2HA mostly associated with the Golgi; however, CteG-2HA also appeared at the host cell plasma membrane, and at 30 or 40 h post-infection this was its predominant localization. This change in the main localization of CteG-2HA was independent of intact microfilaments or microtubules. Ectopic expression of different regions of CteG (656 amino acid residues) in uninfected cells revealed that its first 100 residues contain a Golgi targeting region. Although a C. trachomatis cteG mutant did not display a defect in intracellular multiplication, CteG induced a vacuolar protein sorting defect when expressed in Saccharomyces cerevisiae. This suggested that CteG might function by subverting host cell vesicular transport. Nature Publishing Group UK 2019-04-16 /pmc/articles/PMC6468002/ /pubmed/30992493 http://dx.doi.org/10.1038/s41598-019-42647-3 Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Pais, Sara V.
Key, Charlotte E.
Borges, Vítor
Pereira, Inês S.
Gomes, João Paulo
Fisher, Derek J.
Mota, Luís Jaime
CteG is a Chlamydia trachomatis effector protein that associates with the Golgi complex of infected host cells
title CteG is a Chlamydia trachomatis effector protein that associates with the Golgi complex of infected host cells
title_full CteG is a Chlamydia trachomatis effector protein that associates with the Golgi complex of infected host cells
title_fullStr CteG is a Chlamydia trachomatis effector protein that associates with the Golgi complex of infected host cells
title_full_unstemmed CteG is a Chlamydia trachomatis effector protein that associates with the Golgi complex of infected host cells
title_short CteG is a Chlamydia trachomatis effector protein that associates with the Golgi complex of infected host cells
title_sort cteg is a chlamydia trachomatis effector protein that associates with the golgi complex of infected host cells
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6468002/
https://www.ncbi.nlm.nih.gov/pubmed/30992493
http://dx.doi.org/10.1038/s41598-019-42647-3
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