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Proximity-dependent proteomics of the Chlamydia trachomatis inclusion membrane (revised)

ABSTRACT: Proximity-dependent proteomics of the Chlamydia trachomatis inclusion membrane reveals functional interactions with endoplasmic reticulum exit sites.

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Hela-229 Cell

SUBMITTER: Matthew Monroe

LAB HEAD: Aaron Wright

PROVIDER: PXD012494 | Pride | 2019-08-27

REPOSITORIES: Pride

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			Action	DRS
	Hybiske_H229_Ctrachomatis_16hr_10_18Oct16_Frodo_16-09-09.mgf	Mgf
	Hybiske_H229_Ctrachomatis_16hr_10_18Oct16_Frodo_16-09-09.pride.mgf.gz	Mgf
	Hybiske_H229_Ctrachomatis_16hr_10_18Oct16_Frodo_16-09-09.raw	Raw
	Hybiske_H229_Ctrachomatis_16hr_10_18Oct16_Frodo_16-09-09_msgfplus.mzid.gz	Mzid
	Hybiske_H229_Ctrachomatis_16hr_11_rr_18Oct16_Frodo_16-09-09.mgf	Mgf

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Proximity-dependent proteomics of the Chlamydia trachomatis inclusion membrane reveals functional interactions with endoplasmic reticulum exit sites.

Dickinson Mary S MS Anderson Lindsey N LN Webb-Robertson Bobbie-Jo M BM Hansen Joshua R JR Smith Richard D RD Wright Aaron T AT Hybiske Kevin K

PLoS pathogens 20190403 4

Chlamydia trachomatis is the most common cause of bacterial sexually transmitted infection, responsible for millions of infections each year. Despite this high prevalence, the elucidation of the molecular mechanisms of Chlamydia pathogenesis has been difficult due to limitations in genetic tools and its intracellular developmental cycle. Within a host epithelial cell, chlamydiae replicate within a vacuole called the inclusion. Many Chlamydia-host interactions are thought to be mediated by the In ...[more]

PMID: 30943267

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Project description:Chlamydia trachomatis is the leading cause of bacterial sexually transmitted infections in the US and preventable blindness worldwide. This obligate intracellular pathogen replicates within a membrane-bound inclusion, but how it acquires nutrients from the host while avoiding detection by the innate immune system is incompletely understood. Chlamydia accomplishes this in part through the translocation of a unique set of effectors into the inclusion membrane, the inclusion membrane proteins (Incs). Incs are ideally poised at the host-pathogen interface to reprogram host signaling by redirecting proteins or organelles to the inclusion. Using a combination of co-affinity purification, immunofluorescence confocal imaging, and proteomics, we characterize the interaction between an early-expressed Inc of unknown function, Tri1, and tumor necrosis factor receptor associated factor 7 (TRAF7). TRAF7 is a multi-domain protein with a RING finger ubiquitin ligase domain and a C-terminal WD40 domain, the latter is mutated in a subset of tumors. TRAF7 regulates several innate immune signaling pathways associated with C. trachomatis infection. We demonstrate that Tri1 and TRAF7 specifically interact during infection and that TRAF7 is recruited to the inclusion. We further show that the predicted coiled-coil domain Tri1 is necessary and sufficient to interact with the TRAF7 WD40 domain. Finally, we demonstrate that Tri1 displaces native TRAF7 binding partners, MEKK2 and MEKK3. Together, our results suggest that by displacing the TRAF7 native binding partners MEKK2 and/or MEKK3, Tri1 has the capacity to alter TRAF7 signaling during infection.

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