Targeting eukaryotic Rab proteins: a smart strategy for chlamydial survival and replication

Damiani, Maria Elena; Tudela, Julián A. Gambarte; Capmany, Anahí

doi:10.1111/cmi.12325

Cited by 36 publications

(41 citation statements)

References 61 publications

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“…RAB GTPases are master regulators of vesicle fusion and particular RABs are recruited to inclusions, some of them in a species-specific manner 53 . RAB1, RAB4, RAB11 and RAB14 were recruited to all of the species tested, whereas RAB6 was recruited only to C. trachomatis and RAB10 was recruited only to C. pneumoniae .…”

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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Section: Establishing An Intracellular Nichementioning

confidence: 99%

Chlamydia cell biology and pathogenesis

2016

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“…trachomatis, as for many other intracellular pathogens, have developed different strategies to survive and replicate within infected cells. By recruiting certain Rabs and excluding others, these bacteria avoid degradation in the phagocytic pathway and intercept vesicles carrying host molecules required for bacterial growth (Damiani et al, 2014;Gutierrez, 2013). Although several researchers have explored the participation of Rabs in chlamydial infection, this issue is far from being fully understood.…”

Section: Rab39a Localization To Chlamydial Inclusionsmentioning

confidence: 99%

“…Inclusion growth and bacterial replication depends on the acquisition of nutrients and biosynthetic constituents from the host. Following multiple rounds of replication, reticulate bodies redifferentiate back into elementary bodies and leave infected cells by lysis or extrusion, after which bacteria disseminate and invade neighbouring cells (Bastidas et al, 2013;Damiani et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

The late endocytic Rab39a GTPase regulates multivesicular bodies-chlamydial inclusion interaction and bacterial growth

Tudela

Capmany

Romao

et al. 2015

Journal of Cell Science

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Given their obligate intracellular lifestyle, Chlamydia trachomatis ensure that they have access to multiple host sources of essential lipids by interfering with vesicular transport. These bacteria hijack Rab6-, Rab11-and Rab14-controlled trafficking pathways to acquire sphingomyelin from the Golgi complex. Another important source of sphingolipids, phospholipids and cholesterol are multivesicular bodies (MVBs). Despite their participation in chlamydial inclusion development and bacterial replication, the molecular mechanisms mediating the interaction between MVBs and chlamydial inclusions remain unknown. In the present study, we demonstrate that Rab39a labels a subset of late endocytic vesicles -mainly MVBs -that move along microtubules. Moreover, Rab39a is actively recruited to chlamydial inclusions throughout the pathogen life cycle by a bacterial-driven process that depends on the Rab39a GTP-or GDP-binding state. Interestingly, Rab39a participates in the delivery of MVBs and host sphingolipids to maturing chlamydial inclusions, thereby promoting inclusion growth and bacterial development. Taken together, our findings indicate that Rab39a favours chlamydial replication and infectivity. This is the first report showing that a late endocytic Rab GTPase is involved in chlamydial infection development.

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“…One family of secreted proteins is the inclusion proteins (Incs) which are anchored by their transmembrane domain in the inclusion membrane. It was shown that Incs can specifically interact with transport vesicles through interaction with Rab and Syntaxin proteins (Damiani et al 2014). Furthermore, a specific interaction of IncG with the host cell protein 14-3-3β was shown (Scidmore and Hackstadt 2001).…”

Section: Enrichment Of Anti-apoptotic Proteinsmentioning

confidence: 98%

Subversion of Cell-Autonomous Host Defense by Chlamydia Infection

Fischer

Rudel

2016

Biology of Chlamydia

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Obligate intracellular bacteria entirely depend on the metabolites of their host cell for survival and generation of progeny. Due to their lifestyle inside a eukaryotic cell and the lack of any extracellular niche, they have to perfectly adapt to compartmentalized intracellular environment of the host cell and counteract the numerous defense strategies intrinsically present in all eukaryotic cells. This so-called cell-autonomous defense is present in all cell types encountering Chlamydia infection and is in addition closely linked to the cellular innate immune defense of the mammalian host. Cell type and chlamydial species-restricted mechanisms point a long-term evolutionary adaptation that builds the basis of the currently observed host and cell-type tropism among different Chlamydia species. This review will summarize the current knowledge on the strategies pathogenic Chlamydia species have developed to subvert and overcome the multiple mechanisms by which eukaryotic cells defend themselves against intracellular pathogens.

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Targeting eukaryotic Rab proteins: a smart strategy for chlamydial survival and replication

Cited by 36 publications

References 61 publications

Chlamydia cell biology and pathogenesis

Chlamydia cell biology and pathogenesis

The late endocytic Rab39a GTPase regulates multivesicular bodies-chlamydial inclusion interaction and bacterial growth

Subversion of Cell-Autonomous Host Defense by Chlamydia Infection

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