Depletion of SNAP-23 and Syntaxin 4 alters lipid droplet homeostasis during Chlamydia infection

Authors:

Tiago Monteiro-Brás1,2,3, Jordan Wesolowski1 and Fabienne Paumet1

doi: 10.15698/mic2020.02.707
Volume 7, pp. 46 to 58, published 03/12/2019.

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Affiliations:

1 Department of Microbiology and Immunology, Thomas Jefferson University, Philadelphia, PA, USA 19107.

2 Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, 4710-057 Braga, Portugal.

3 ICVS/3B’s, PT Government Associate Laboratory, 4710-057, Braga/Guimarães, Portugal.

Keywords: 

lipid droplets, Chlamydia, SNARE, intracellular bacteria, inclusion

Corresponding Author(s):

Fabienne Paumet, 233 South 10th Street, Bluemle Life Sciences building room 750, Philadelphia, PA 19104; Phone: 215-503-8567; Fax: 215-923-6852; Fabienne.Paumet@Jefferson.edu Jordan Wesolowski, 233 South 10th Street, Bluemle Life Sciences building room 750, Philadelphia, PA 19104; Phone: 215-503-8566; Fax: 215-923-6852; Jordan.Wesolowski@Jefferson.edu

Conflict of interest statement:

The authors declare no conflicts of interest.

Please cite this article as:

Tiago Monteiro-Brás, Jordan Wesolowski and Fabienne Paumet (2019). Depletion of SNAP-23 and Syntaxin 4 alters lipid droplet homeostasis during Chlamydia infection. Microbial Cell 7(2): 46-58. doi: 10.15698/mic2020.02.707

© 2019 Monteiro-Brás et al. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and re-production in any medium, provided the original author and source are acknowledged.

Abstract:

Chlamydia trachomatis is an obligate intracellular pathogen that replicates inside a parasitic vacuole called the inclusion. The nascent inclusion is derived from the host plasma membrane and serves as a platform from which Chlamydia controls interactions with the host microenvironment. To survive inside the host cell, Chlamydia scavenges for nutrients and lipids by recruiting and/or fusing with various cellular compartments. The mechanisms by which these events occur are poorly understood but require host proteins such as the SNARE proteins (SNAP (Soluble N-ethylmaleimide-sensitive factor attachment protein) Receptor). Here, we show that SNAP-23 and Syntaxin 4, two plasma membrane SNAREs, are recruited to the inclusion and play an important role in Chlamydia development. Knocking down SNAP-23 and Syntaxin 4 by CRISPR-Cas9 reduces the amount of infectious progeny. We then demonstrate that the loss of both of these SNARE proteins results in the dysregulation of Chlamydia-induced lipid droplets, indicating that both SNAP-23 and Syntaxin 4 play a critical role in lipid droplet homeostasis during Chlamydia infection. Ultimately, our data highlights the importance of lipid droplets and their regulation in Chlamydia development.