Rho GTPases as pathogen targets: Focus on curable sexually transmitted infections

Quintero, Cristián; Tudela, Julián Gambarte; Damiani, Marı́a Teresa

doi:10.4161/21541248.2014.991233

Cited by 13 publications

(10 citation statements)

References 123 publications

(111 reference statements)

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“…By reducing microtubule de-polymerisation this allows Salmonella to promote tubular lysosomes (endosomal tubules), in conjunction with other proteins such as SifA, increasing fusion events with endosomal vesicles carrying in nutrients from the extracellular environment. Rho GTPases are a common target of bacterial pathogens [ 49 , 50 ] and further work is required to determine whether SseJ’s effect on cellular microtubules is mediated through RhoA or RhoC.…”

Section: Discussionmentioning

confidence: 99%

The Salmonella effector SseJ disrupts microtubule dynamics when ectopically expressed in normal rat kidney cells

et al. 2017

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Salmonella effector protein SseJ is secreted by Salmonella into the host cell cytoplasm where it can then modify host cell processes. Whilst host cell small GTPase RhoA has previously been shown to activate the acyl-transferase activity of SseJ we show here an un-described effect of SseJ protein production upon microtubule dynamism. SseJ prevents microtubule collapse and this is independent of SseJ’s acyl-transferase activity. We speculate that the effects of SseJ on microtubules would be mediated via its known interactions with the small GTPases of the Rho family.

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Section: Discussionmentioning

confidence: 99%

The Salmonella effector SseJ disrupts microtubule dynamics when ectopically expressed in normal rat kidney cells

et al. 2017

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“…Once internalized, they hijack the molecular machinery of the infected cell not only to prevent their own degradation in the phagocytic pathway, but also to create a favorable intracellular environment for growth and replication. Cristi an Quintero, Juli an Gambarte, Mar ıa Damiani 39 focus their attention on the role of Rho proteins on four curable, sexually transmitted infections, Chlamydia trachomatis, Neisseria gonorrhoeae, Trichomonas vaginalis and Treponema pallidum.…”

Section: Rho Gtpase As Pathogen Targets; Therapeutic Perspectivesmentioning

confidence: 99%

Rho GTPases at the crossroad of signaling networks in mammals

Hervé

Bourmeyster

2015

Small GTPases

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“…The antibacterial cathelicidin LL-37 increases the cellular stiffness of lung epithelial cells resulting in reduced uptake of Pseudomonas aeruginosa (Byfield et al, 2011). Actin polymerization, focal adhesion signaling, and Rho GTPase activity play important roles in the infection of a wide variety of bacteria (Galan & Zhou, 2000;Prashar et al, 2018;Quintero, Tudela, & Damiani, 2015); thus, while the effects of tissue stiffness on bacterial pathogenesis have thus far not been well studied, we hypothesize that matrix mechanics may be a critical regulator for a range of microbial infections.…”

Section: Role Of Mechanical Forces In Bacterial Pathogenesismentioning

confidence: 98%

Matrix stiffness regulates endosomal escape of uropathogenicE. coli

Moorthy

Byfield

Janmey

et al. 2020

Cellular Microbiology

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Uropathogenic E. coli (UPEC) infection in vivo is characterized by invasion of bladder umbrella epithelial cells followed by endosomal escape and proliferation in the cytoplasm to form intracellular bacterial communities. By contrast, UPEC infection in tissue culture models results in bacteria being trapped within Lamp1‐positive endosomes where proliferation is limited. Pharmacological disruption of the actin cytoskeleton has been shown to facilitate UPEC endosomal escape in vitro and extracellular matrix stiffness is a well‐characterized physiological regulator of actin dynamics; therefore, we hypothesized that substrate stiffness may play a role in UPEC endosomal escape. Using functionalized polyacrylamide substrates, we found that at physiological stiffness, UPEC escaped the endosome and proliferated rapidly in the cytoplasm of bladder epithelial cells. Dissection of the cytoskeletal signaling pathway demonstrated that inhibition of the Rho GTPase RhoB or its effector PRK1 was sufficient to increase cytoplasmic bacterial growth and that RhoB protein level was significantly reduced at physiological stiffness. Our data suggest that tissue stiffness is a critical regulator of intracellular bacterial growth. Due to the ease of doing genetic and pharmacological manipulations in cell culture, this model system may provide a useful tool for performing mechanistic studies on the intracellular life cycle of uropathogens.

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Rho GTPases as pathogen targets: Focus on curable sexually transmitted infections

Cited by 13 publications

References 123 publications

The Salmonella effector SseJ disrupts microtubule dynamics when ectopically expressed in normal rat kidney cells

The Salmonella effector SseJ disrupts microtubule dynamics when ectopically expressed in normal rat kidney cells

Rho GTPases at the crossroad of signaling networks in mammals

Matrix stiffness regulates endosomal escape of uropathogenicE. coli

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