The DUF582 Proteins of Chlamydia trachomatis Bind to Components of the ESCRT Machinery, Which Is Dispensable for Bacterial Growth In vitro

Vromman, François; Perrinet, Stéphanie; Gehre, Lena; Subtil, Agathe

doi:10.3389/fcimb.2016.00123

Cited by 19 publications

(23 citation statements)

References 36 publications

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“…The involvement of these key abscission proteins parallels similar requirements for viral exit strategies, including HIV budding from the host cell [18,38], and therefore abscission proteins may be a common target of intracellular pathogens faced with the challenge of exiting cells by a membrane-mediated route. These findings are even more intriguing in light of recent data, demonstrating an interaction between ESCRT-I protein TSG101, and a chlamydial effector protein, CT619 [39]. TSG101, with its interaction partner ALIX, are crucial to normal kinetics and progression of cell abscission.…”

Section: Discussionmentioning

confidence: 98%

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

Zuck

Hybiske

2019

Microorganisms

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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.

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Section: Discussionmentioning

confidence: 98%

“…TSG101, with its interaction partner ALIX, are crucial to normal kinetics and progression of cell abscission. Without any known function of TSG101 in chlamydial development in vitro, it is possible that these proteins are targeted by Chlamydia specifically to facilitate exit via extrusion [39].…”

Section: Discussionmentioning

confidence: 99%

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

Zuck

Hybiske

2019

Microorganisms

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“…ESCRT (endosomal sorting complex required for transport) plays an important role in exosome biogenesis and MVB sorting (53). Bacterial recruitment of the ESCRT machinery is critical for maintaining the productive life cycle of Chlamydia (54). However, chlamydial growth is severely impaired in DCs (46).…”

Section: Discussionmentioning

confidence: 99%

Chlamydia psittaci -Infected Dendritic Cells Communicate with NK Cells via Exosomes To Activate Antibacterial Immunity

et al. 2019

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Dendritic cells (DCs) and natural killer (NK) cells are critically involved in the early response against various bacterial microbes. Functional activation of infected DCs and NK cell-mediated gamma interferon (IFN-γ) secretion essentially contribute to the protective immunity against Chlamydia. How DCs and NK cells cooperate during the antichlamydial response is not fully understood. Therefore, in the present study, we investigated the functional interplay between Chlamydia-infected DCs and NK cells. Our biochemical and cell biological experiments show that Chlamydia psittaci-infected DCs display enhanced exosome release. We find that such extracellular vesicles (referred to as dexosomes) do not contain infectious bacterial material but strongly induce IFN-γ production by NK cells. This directly affects C. psittaci growth in infected target cells. Furthermore, NK cell-released IFN-γ in cooperation with tumor necrosis factor alpha (TNF-α) and/or dexosomes augments apoptosis of both noninfected and infected epithelial cells. Thus, the combined effect of dexosomes and proinflammatory cytokines restricts C. psittaci growth and attenuates bacterial subversion of apoptotic host cell death. In conclusion, this provides new insights into the functional cooperation between DCs, dexosomes, and NK cells in the early steps of antichlamydial defense.

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“…aOnly C. trachomatis proteins reported to be experimentally detected in the inclusion membrane, inclusion lumen, host cell cytoplasm or nucleus are listed. In addition, there is functional evidence for secretion and effector role of CT166 ( Chlamydia cytotoxin targeting RAC1 that might contribute for downmodulating actin cytoskeleton changes during chlamydial invasion of host cells [197, 199]), CT619/CTL0883 and CT712/CTL0081 (as CT620/CTL0884, CT621/CTL0885, and CT711/CTL0080, listed in Table 2, these two proteins contain the Chlamydiacea -unique DUF582 domain and bind components of the ESCRT machinery [212, 214]), and CT847/CTL0217 (binds GCIP [229]) in the host cell cytoplasm, and of GlgB, GlgP, MalQ and MrsA in the inclusion lumen [14, 289]. See list of abbreviations and main text for abbreviations and protein nomenclature, respectively.…”

Section: Trachomatis Non-inc Proteins Delivered To the Outside Of mentioning

confidence: 99%

The multiple functions of the numerous Chlamydia trachomatis secreted proteins: the tip of the iceberg

Bugalhão¹,

Mota²

2019

Microb Cell

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Chlamydia trachomatis serovars are obligate intracellular bacterial pathogens mainly causing ocular and urogenital infections that affect millions of people worldwide and which can lead to blindness or sterility. They reside and multiply intracellularly within a membrane-bound vacuolar compartment, known as inclusion, and are characterized by a developmental cycle involving two morphologically and physiologically distinct chlamydial forms. Completion of the developmental cycle involves the secretion of > 70 C. trachomatis proteins that function in the host cell cytoplasm and nucleus, in the inclusion membrane and lumen, and in the extracellular milieu. These proteins can, for example, interfere with the host cell cytoskeleton, vesicular and non-vesicular transport, metabolism, and immune signalling. Generally, this promotes C. trachomatis invasion into, and escape from, host cells, the acquisition of nutrients by the chlamydiae, and evasion of cell-autonomous, humoral and cellular innate immunity. Here, we present an in-depth review on the current knowledge and outstanding questions about these C. trachomatis secreted proteins.

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The DUF582 Proteins of Chlamydia trachomatis Bind to Components of the ESCRT Machinery, Which Is Dispensable for Bacterial Growth In vitro

Cited by 19 publications

References 36 publications

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

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

Chlamydia psittaci -Infected Dendritic Cells Communicate with NK Cells via Exosomes To Activate Antibacterial Immunity

The multiple functions of the numerous Chlamydia trachomatis secreted proteins: the tip of the iceberg

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