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The trans-Golgi SNARE syntaxin 10 is required for optimal development of Chlamydia trachomatis

Chlamydia trachomatis, an obligate intracellular pathogen, grows inside of a vacuole, termed the inclusion. Within the inclusion, the organisms differentiate from the infectious elementary body (EB) into the reticulate body (RB). The RB communicates with the host cell through the inclusion membrane...

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Autores principales: Lucas, Andrea L., Ouellette, Scot P., Kabeiseman, Emily J., Cichos, Kyle H., Rucks, Elizabeth A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4585193/
https://www.ncbi.nlm.nih.gov/pubmed/26442221
http://dx.doi.org/10.3389/fcimb.2015.00068
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author Lucas, Andrea L.
Ouellette, Scot P.
Kabeiseman, Emily J.
Cichos, Kyle H.
Rucks, Elizabeth A.
author_facet Lucas, Andrea L.
Ouellette, Scot P.
Kabeiseman, Emily J.
Cichos, Kyle H.
Rucks, Elizabeth A.
author_sort Lucas, Andrea L.
collection PubMed
description Chlamydia trachomatis, an obligate intracellular pathogen, grows inside of a vacuole, termed the inclusion. Within the inclusion, the organisms differentiate from the infectious elementary body (EB) into the reticulate body (RB). The RB communicates with the host cell through the inclusion membrane to obtain the nutrients necessary to divide, thus expanding the chlamydial population. At late time points within the developmental cycle, the RBs respond to unknown molecular signals to redifferentiate into infectious EBs to perpetuate the infection cycle. One strategy for Chlamydia to obtain necessary nutrients and metabolites from the host is to intercept host vesicular trafficking pathways. In this study we demonstrate that a trans-Golgi soluble N-ethylmaleimide–sensitive factor attachment protein (SNARE), syntaxin 10, and/or syntaxin 10-associated Golgi elements colocalize with the chlamydial inclusion. We hypothesized that Chlamydia utilizes the molecular machinery of syntaxin 10 at the inclusion membrane to intercept specific vesicular trafficking pathways in order to create and maintain an optimal intra-inclusion environment. To test this hypothesis, we used siRNA knockdown of syntaxin 10 to examine the impact of the loss of syntaxin 10 on chlamydial growth and development. Our results demonstrate that loss of syntaxin 10 leads to defects in normal chlamydial maturation including: variable inclusion size with fewer chlamydial organisms per inclusion, fewer infectious progeny, and delayed or halted RB-EB differentiation. These defects in chlamydial development correlate with an overabundance of NBD-lipid retained by inclusions cultured in syntaxin 10 knockdown cells. Overall, loss of syntaxin 10 at the inclusion membrane negatively affects Chlamydia. Understanding host machinery involved in maintaining an optimal inclusion environment to support chlamydial growth and development is critical toward understanding the molecular signals involved in successful progression through the chlamydial developmental cycle.
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spelling pubmed-45851932015-10-05 The trans-Golgi SNARE syntaxin 10 is required for optimal development of Chlamydia trachomatis Lucas, Andrea L. Ouellette, Scot P. Kabeiseman, Emily J. Cichos, Kyle H. Rucks, Elizabeth A. Front Cell Infect Microbiol Microbiology Chlamydia trachomatis, an obligate intracellular pathogen, grows inside of a vacuole, termed the inclusion. Within the inclusion, the organisms differentiate from the infectious elementary body (EB) into the reticulate body (RB). The RB communicates with the host cell through the inclusion membrane to obtain the nutrients necessary to divide, thus expanding the chlamydial population. At late time points within the developmental cycle, the RBs respond to unknown molecular signals to redifferentiate into infectious EBs to perpetuate the infection cycle. One strategy for Chlamydia to obtain necessary nutrients and metabolites from the host is to intercept host vesicular trafficking pathways. In this study we demonstrate that a trans-Golgi soluble N-ethylmaleimide–sensitive factor attachment protein (SNARE), syntaxin 10, and/or syntaxin 10-associated Golgi elements colocalize with the chlamydial inclusion. We hypothesized that Chlamydia utilizes the molecular machinery of syntaxin 10 at the inclusion membrane to intercept specific vesicular trafficking pathways in order to create and maintain an optimal intra-inclusion environment. To test this hypothesis, we used siRNA knockdown of syntaxin 10 to examine the impact of the loss of syntaxin 10 on chlamydial growth and development. Our results demonstrate that loss of syntaxin 10 leads to defects in normal chlamydial maturation including: variable inclusion size with fewer chlamydial organisms per inclusion, fewer infectious progeny, and delayed or halted RB-EB differentiation. These defects in chlamydial development correlate with an overabundance of NBD-lipid retained by inclusions cultured in syntaxin 10 knockdown cells. Overall, loss of syntaxin 10 at the inclusion membrane negatively affects Chlamydia. Understanding host machinery involved in maintaining an optimal inclusion environment to support chlamydial growth and development is critical toward understanding the molecular signals involved in successful progression through the chlamydial developmental cycle. Frontiers Media S.A. 2015-09-25 /pmc/articles/PMC4585193/ /pubmed/26442221 http://dx.doi.org/10.3389/fcimb.2015.00068 Text en Copyright © 2015 Lucas, Ouellette, Kabeiseman, Cichos and Rucks. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Microbiology
Lucas, Andrea L.
Ouellette, Scot P.
Kabeiseman, Emily J.
Cichos, Kyle H.
Rucks, Elizabeth A.
The trans-Golgi SNARE syntaxin 10 is required for optimal development of Chlamydia trachomatis
title The trans-Golgi SNARE syntaxin 10 is required for optimal development of Chlamydia trachomatis
title_full The trans-Golgi SNARE syntaxin 10 is required for optimal development of Chlamydia trachomatis
title_fullStr The trans-Golgi SNARE syntaxin 10 is required for optimal development of Chlamydia trachomatis
title_full_unstemmed The trans-Golgi SNARE syntaxin 10 is required for optimal development of Chlamydia trachomatis
title_short The trans-Golgi SNARE syntaxin 10 is required for optimal development of Chlamydia trachomatis
title_sort trans-golgi snare syntaxin 10 is required for optimal development of chlamydia trachomatis
topic Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4585193/
https://www.ncbi.nlm.nih.gov/pubmed/26442221
http://dx.doi.org/10.3389/fcimb.2015.00068
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