<italic toggle="yes">Chlamydia</italic> Hijacks ARF GTPases To Coordinate Microtubule Posttranslational Modifications and Golgi Complex Positioning

ABSTRACT The intracellular bacterium Chlamydia trachomatis develops in a parasitic compartment called the inclusion. Posttranslationally modified microtubules encase the inclusion, controlling the positioning of Golgi complex fragments around the inclusion. The molecular mechanisms by which Chlamydi...

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Autores principales:	Jordan Wesolowski, Mary M. Weber, Agata Nawrotek, Cheryl A. Dooley, Mike Calderon, Claudette M. St. Croix, Ted Hackstadt, Jacqueline Cherfils, Fabienne Paumet
Formato:	article
Lenguaje:	EN
Publicado:	American Society for Microbiology 2017
Materias:	ARF GTPase actin CT813 Chlamydia trachomatis Golgi complex inclusion protein Microbiology QR1-502
Acceso en línea:	https://doaj.org/article/1b0aa9e0ba83433dbf1e26bc29d92500
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spelling	oai:doaj.org-article:1b0aa9e0ba83433dbf1e26bc29d925002021-11-15T15:51:29Z<italic toggle="yes">Chlamydia</italic> Hijacks ARF GTPases To Coordinate Microtubule Posttranslational Modifications and Golgi Complex Positioning10.1128/mBio.02280-162150-7511https://doaj.org/article/1b0aa9e0ba83433dbf1e26bc29d925002017-07-01T00:00:00Zhttps://journals.asm.org/doi/10.1128/mBio.02280-16https://doaj.org/toc/2150-7511ABSTRACT The intracellular bacterium Chlamydia trachomatis develops in a parasitic compartment called the inclusion. Posttranslationally modified microtubules encase the inclusion, controlling the positioning of Golgi complex fragments around the inclusion. The molecular mechanisms by which Chlamydia coopts the host cytoskeleton and the Golgi complex to sustain its infectious compartment are unknown. Here, using a genetically modified Chlamydia strain, we discovered that both posttranslationally modified microtubules and Golgi complex positioning around the inclusion are controlled by the chlamydial inclusion protein CT813/CTL0184/InaC and host ARF GTPases. CT813 recruits ARF1 and ARF4 to the inclusion membrane, where they induce posttranslationally modified microtubules. Similarly, both ARF isoforms are required for the repositioning of Golgi complex fragments around the inclusion. We demonstrate that CT813 directly recruits ARF GTPases on the inclusion membrane and plays a pivotal role in their activation. Together, these results reveal that Chlamydia uses CT813 to hijack ARF GTPases to couple posttranslationally modified microtubules and Golgi complex repositioning at the inclusion. IMPORTANCE Chlamydia trachomatis is an important cause of morbidity and a significant economic burden in the world. However, how Chlamydia develops its intracellular compartment, the so-called inclusion, is poorly understood. Using genetically engineered Chlamydia mutants, we discovered that the effector protein CT813 recruits and activates host ADP-ribosylation factor 1 (ARF1) and ARF4 to regulate microtubules. In this context, CT813 acts as a molecular platform that induces the posttranslational modification of microtubules around the inclusion. These cages are then used to reposition the Golgi complex during infection and promote the development of the inclusion. This study provides the first evidence that ARF1 and ARF4 play critical roles in controlling posttranslationally modified microtubules around the inclusion and that Chlamydia trachomatis hijacks this novel function of ARF to reposition the Golgi complex.Jordan WesolowskiMary M. WeberAgata NawrotekCheryl A. DooleyMike CalderonClaudette M. St. CroixTed HackstadtJacqueline CherfilsFabienne PaumetAmerican Society for MicrobiologyarticleARF GTPaseactinCT813Chlamydia trachomatisGolgi complexinclusion proteinMicrobiologyQR1-502ENmBio, Vol 8, Iss 3 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	ARF GTPase actin CT813 Chlamydia trachomatis Golgi complex inclusion protein Microbiology QR1-502
spellingShingle	ARF GTPase actin CT813 Chlamydia trachomatis Golgi complex inclusion protein Microbiology QR1-502 Jordan Wesolowski Mary M. Weber Agata Nawrotek Cheryl A. Dooley Mike Calderon Claudette M. St. Croix Ted Hackstadt Jacqueline Cherfils Fabienne Paumet <italic toggle="yes">Chlamydia</italic> Hijacks ARF GTPases To Coordinate Microtubule Posttranslational Modifications and Golgi Complex Positioning
description	ABSTRACT The intracellular bacterium Chlamydia trachomatis develops in a parasitic compartment called the inclusion. Posttranslationally modified microtubules encase the inclusion, controlling the positioning of Golgi complex fragments around the inclusion. The molecular mechanisms by which Chlamydia coopts the host cytoskeleton and the Golgi complex to sustain its infectious compartment are unknown. Here, using a genetically modified Chlamydia strain, we discovered that both posttranslationally modified microtubules and Golgi complex positioning around the inclusion are controlled by the chlamydial inclusion protein CT813/CTL0184/InaC and host ARF GTPases. CT813 recruits ARF1 and ARF4 to the inclusion membrane, where they induce posttranslationally modified microtubules. Similarly, both ARF isoforms are required for the repositioning of Golgi complex fragments around the inclusion. We demonstrate that CT813 directly recruits ARF GTPases on the inclusion membrane and plays a pivotal role in their activation. Together, these results reveal that Chlamydia uses CT813 to hijack ARF GTPases to couple posttranslationally modified microtubules and Golgi complex repositioning at the inclusion. IMPORTANCE Chlamydia trachomatis is an important cause of morbidity and a significant economic burden in the world. However, how Chlamydia develops its intracellular compartment, the so-called inclusion, is poorly understood. Using genetically engineered Chlamydia mutants, we discovered that the effector protein CT813 recruits and activates host ADP-ribosylation factor 1 (ARF1) and ARF4 to regulate microtubules. In this context, CT813 acts as a molecular platform that induces the posttranslational modification of microtubules around the inclusion. These cages are then used to reposition the Golgi complex during infection and promote the development of the inclusion. This study provides the first evidence that ARF1 and ARF4 play critical roles in controlling posttranslationally modified microtubules around the inclusion and that Chlamydia trachomatis hijacks this novel function of ARF to reposition the Golgi complex.
format	article
author	Jordan Wesolowski Mary M. Weber Agata Nawrotek Cheryl A. Dooley Mike Calderon Claudette M. St. Croix Ted Hackstadt Jacqueline Cherfils Fabienne Paumet
author_facet	Jordan Wesolowski Mary M. Weber Agata Nawrotek Cheryl A. Dooley Mike Calderon Claudette M. St. Croix Ted Hackstadt Jacqueline Cherfils Fabienne Paumet
author_sort	Jordan Wesolowski
title	<italic toggle="yes">Chlamydia</italic> Hijacks ARF GTPases To Coordinate Microtubule Posttranslational Modifications and Golgi Complex Positioning
title_short	<italic toggle="yes">Chlamydia</italic> Hijacks ARF GTPases To Coordinate Microtubule Posttranslational Modifications and Golgi Complex Positioning
title_full	<italic toggle="yes">Chlamydia</italic> Hijacks ARF GTPases To Coordinate Microtubule Posttranslational Modifications and Golgi Complex Positioning
title_fullStr	<italic toggle="yes">Chlamydia</italic> Hijacks ARF GTPases To Coordinate Microtubule Posttranslational Modifications and Golgi Complex Positioning
title_full_unstemmed	<italic toggle="yes">Chlamydia</italic> Hijacks ARF GTPases To Coordinate Microtubule Posttranslational Modifications and Golgi Complex Positioning
title_sort	<italic toggle="yes">chlamydia</italic> hijacks arf gtpases to coordinate microtubule posttranslational modifications and golgi complex positioning
publisher	American Society for Microbiology
publishDate	2017
url	https://doaj.org/article/1b0aa9e0ba83433dbf1e26bc29d92500
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<italic toggle="yes">Chlamydia</italic> Hijacks ARF GTPases To Coordinate Microtubule Posttranslational Modifications and Golgi Complex Positioning

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