Chlamydia psittaci inclusion membrane protein IncB associates with host protein Snapin

Böcker, Selina; Heurich, Adeline; Franke, Claudia; Monajembashi, Shamci; Sachse, Konrad; Saluz, Hans Peter; Hänel, F.

doi:10.1016/j.ijmm.2014.03.005

Cited by 19 publications

(19 citation statements)

References 27 publications

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“…One of the few Inc proteins having orthologues in both C. trachomatis and C. psittaci is IncB (Voigt, Schofl, & Saluz, ). For IncB of C. psittaci , but not for C. trachomatis , binding to the human protein Snapin has been shown, indicating that IncB at least partially mediates species‐specific interactions with a human host cell (Bocker et al, ).…”

Section: Discussionmentioning

confidence: 99%

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The cellular ceramide transport protein CERT promotesChlamydia psittaciinfection and controls bacterial sphingolipid uptake

Koch-Edelmann

Banhart

Saied

et al. 2017

Cellular Microbiology

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Chlamydiaceae are bacterial pathogens that cause diverse diseases in humans and animals. Despite their broad host and tissue tropism, all Chlamydia species share an obligate intracellular cycle of development and have evolved sophisticated mechanisms to interact with their eukaryotic host cells. Here, we have analysed interactions of the zoonotic pathogen Chlamydia psittaci with a human epithelial cell line. We found that C. psittaci recruits the ceramide transport protein (CERT) to its inclusion. Chemical inhibition and CRISPR/Cas9-mediated knockout of CERT showed that CERT is a crucial factor for C. psittaci infections thereby affecting different stages of the infection including inclusion growth and infectious progeny formation. Interestingly, the uptake of fluorescently labelled sphingolipids in bacteria inside the inclusion was accelerated in CERT-knockout cells indicating that C. psittaci can exploit CERT-independent sphingolipid uptake pathways. Moreover, the CERT-specific inhibitor HPA-12 strongly diminished sphingolipid transport to inclusions of infected CERT-knockout cells, suggesting that other HPA-12-sensitive factors are involved in sphingolipid trafficking to C. psittaci. Further analysis is required to decipher these interactions and to understand their contributions to bacterial development, host range, tissue tropism, and disease outcome.

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Section: Discussionmentioning

confidence: 99%

“…How C. psittaci interacts with the lipid transport machinery in human host cells has not been addressed. So far, only few interactions between C. psittaci and human cells have been characterised (Bocker et al, ; Borth et al, ; Knittler et al, ; Mojica et al, ).…”

Section: Introductionmentioning

confidence: 99%

The cellular ceramide transport protein CERT promotesChlamydia psittaciinfection and controls bacterial sphingolipid uptake

Koch-Edelmann

Banhart

Saied

et al. 2017

Cellular Microbiology

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“…CT850 from C. trachomatis can directly bind to dynein light chain 1 (DYNLT1) to promote the positioning of the inclusion at the MTOC 51 . IncB from C. psittaci binds to Snapin, a protein that associates with host SNARE proteins (soluble N -ethylmaleimide-sensitive factor attachment protein receptor proteins) 52 . As Snapin can bind to both IncB and to dynein, it is possible that IncB–Snapin interactions connect the inclusion to the dynein motor complex for transport.…”

Section: Establishing An Intracellular Nichementioning

confidence: 99%

Chlamydia cell biology and pathogenesis

2016

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Chlamydia spp. are important causes of human disease for which no effective vaccine exists. These obligate intracellular pathogens replicate in a specialized membrane compartment and use a large arsenal of secreted effectors to survive in the hostile intracellular environment of the host. In this Review, we summarize the progress in decoding the interactions between Chlamydia spp. and their hosts that has been made possible by recent technological advances in chlamydial proteomics and genetics. The field is now poised to decipher the molecular mechanisms that underlie the intimate interactions between Chlamydia spp. and their hosts, which will open up many exciting avenues of research for these medically important pathogens.

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“…These early vacuoles translocate via the cytoskeleton to the perinuclear region, where the microtubule‐organizing center (MTOC) is localized , and RBs multiply by binary fission. The chlamydial Inc proteins (e.g., IncA and IncB), which are incorporated in the inclusion membrane via the T3SS , seem to be central regulators of pathogen–host interactions targeting various host cellular functions . Inc proteins are characterized by a hydrophobic domain (containing ≥40 amino acids) that is thought to span cellular membranes twice .…”

Section: Chlamydia Psittaci–host Cell Interaction—attachment Intracementioning

confidence: 99%

“…In light of this, IncA has been proposed to be involved in the homotypic fusion of inclusion membranes . Two different publications on C. psittaci have described dynein motor proteins as well as the host protein G3BP1 as possible cellular IncB‐/IncA–interaction partners . The cellular IncA‐binding protein G3BP1 contains RNase activity, which is dependent on phosphorylation, and cleaves the untranslated 3′ end of the human c‐myc transcript .…”

Section: Chlamydia Psittaci–host Cell Interaction—attachment Intracementioning

confidence: 99%

Chlamydia–host cell interaction not only from a bird's eye view: some lessons from Chlamydia psittaci

et al. 2016

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Edited by Wilhelm JustChlamydia psittaci causes psittacosis/ornithosis in birds and is an economically important pathogen for poultry farming. It also infects nonavian domestic animals as well as rodents, and is a zoonotic human pathogen responsible for atypical pneumonia. The bacterium efficiently disseminates in host organisms causing pulmonary and systemic disease. Its rapid entry, fast replication cycle, and tight control of intracellular transport routes contribute to the host-to-host transmission and efficient growth observed with C. psittaci. Recent studies have revealed that the pathogen copes better than other chlamydial strains with proinflammatory effectors produced during the early immune reaction of infected hosts. These features likely contribute to successful infections and might explain the potent adaptation and evasion characteristics of the agent. Current findings on cell-autonomous, innate, and adaptive defenses against C. psittaci provide novel insights into the concerted immune mechanisms involved in the clearance of the pathogen. Further in-depth studies on C. psittaci and other related agents in cellular as well as animal models are needed to develop more efficient antichlamydial therapies and vaccination strategies.

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Chlamydia psittaci inclusion membrane protein IncB associates with host protein Snapin

Cited by 19 publications

References 27 publications

The cellular ceramide transport protein CERT promotesChlamydia psittaciinfection and controls bacterial sphingolipid uptake

The cellular ceramide transport protein CERT promotesChlamydia psittaciinfection and controls bacterial sphingolipid uptake

Chlamydia cell biology and pathogenesis

Chlamydia–host cell interaction not only from a bird's eye view: some lessons from Chlamydia psittaci

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