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Open AccessArticle

The Chlamydia trachomatis Extrusion Exit Mechanism Is Regulated by Host Abscission Proteins

1
Department of Medicine, Division of Allergy and Infectious Diseases, Center for Emerging and Reemerging Infectious Disease (CERID), University of Washington, Seattle, WA 98109, USA
2
Division of Infectious Diseases and Immunity, School of Public Health, University of California, Berkeley, CA 94720, USA
*
Author to whom correspondence should be addressed.
Microorganisms 2019, 7(5), 149; https://doi.org/10.3390/microorganisms7050149
Received: 23 April 2019 / Revised: 21 May 2019 / Accepted: 22 May 2019 / Published: 25 May 2019
(This article belongs to the Special Issue Chlamydiae and Chlamydia like Bacteria)
The cellular exit strategies of intracellular pathogens have a direct impact on microbial dissemination, transmission, and engagement of immune responses of the host. Chlamydia exit their host via a budding mechanism called extrusion, which offers protective benefits to Chlamydia as they navigate their extracellular environment. Many intracellular pathogens co-opt cellular abscission machinery to facilitate cell exit, which is utilized to perform scission of two newly formed daughter cells following mitosis. Similar to viral budding exit strategies, we hypothesize that an abscission-like mechanism is required to physically sever the chlamydial extrusion from the host cell, co-opting the membrane fission activities of the endosomal sorting complex required for transport (ESCRT) family of proteins that are necessary for cellular scission events, including abscission. To test this, C. trachomatis L2-infected HeLa cells were depleted of key abscission machinery proteins charged multivesicle body protein 4b (CHMP4B), ALIX, centrosome protein 55 (CEP55), or vacuolar protein sorting-associated protein 4A (VPS4A), using RNA interference (RNAi). Over 50% reduction in extrusion formation was achieved by depletion of CHMP4B, VPS4A, and ALIX, but no effect on extrusion was observed with CEP55 depletion. These results demonstrate a role for abscission machinery in C. trachomatis extrusion from the host cell, with ALIX, VPS4A and CHMP4B playing key functional roles in optimal extrusion release. View Full-Text
Keywords: Chlamydia trachomatis; extrusion; abscission Chlamydia trachomatis; extrusion; abscission
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MDPI and ACS Style

Zuck, M.; Hybiske, K. The Chlamydia trachomatis Extrusion Exit Mechanism Is Regulated by Host Abscission Proteins. Microorganisms 2019, 7, 149.

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