<i>Yersinia enterocolitica</i> differentially modulates RhoG activity in host cells

Roppenser, Bernhard; Röder, A.; Hentschke, Moritz; Ruckdeschel, Klaus; Aepfelbacher, Martin

doi:10.1242/jcs.040345

Cited by 34 publications

(41 citation statements)

References 55 publications

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“…5C). This result was consistent with (i) RhoG being inactivated by the action of Y. pseudotuberculosis YopE and (ii) previous observations of Y. enterocolitica YopE's RhoG GAP activity (42). Interestingly, cytoplasmic levels of RhoG-ELMO FRET (i.e., activation at regions without bound bacteria) remained relatively unchanged (Fig.…”

Section: Resultssupporting

confidence: 92%

“…3A). No such biosensor has been reported, as RhoG activation has been assayed either by IP experiments (27) or by relocalization of an effector (42). While useful for examining activity in bulk, IP methods give no information about localized GTPase activity, and relocalization methods do not directly measure activity.…”

Section: Resultsmentioning

confidence: 99%

“…Localization of GFP fusions at the nascent phagosome was visualized as described for panel A. Scale bars (applicable to all images within the respective panels) ϭ 3 m. (42). The FRET biosensor was used to assess if the activation of RhoG in response to invasin-mediated signaling was localized.…”

Section: Resultsmentioning

confidence: 99%

“…This connection is particularly intriguing because Y. pseudotuberculosis invasin binds to several ␤1 integrins. Additionally, a previous study has indicated that the related organism Y. enterocolitica can modulate RhoG activity (42). Interestingly, RhoG plays a critical role in proper neutrophil function since it has been shown to be necessary for efficient generation of reactive oxygen species (ROS) by neutrophils (7).…”

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confidence: 99%

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Yersinia pseudotuberculosisVirulence Determinants Invasin, YopE, and YopT Modulate RhoG Activity and Localization

Mohammadi

Isberg

2009

Infect Immun

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Section: Resultssupporting

confidence: 92%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

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Yersinia pseudotuberculosisVirulence Determinants Invasin, YopE, and YopT Modulate RhoG Activity and Localization

Mohammadi

Isberg

2009

Infect Immun

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“…In physiological conditions, microbes coming into contact with professional phagocytes will probably be coated with multiple opsonising molecules leading to activation of a variety of signalling pathways (Underhill and Ozinsky, 2002). Subversion of RhoG activity during cell invasion by bacterial pathogens, such as Salmonella enterica (Patel and Galan, 2006) and pathogenic Yersinia species (Mohammadi and Isberg, 2009;Roppenser et al, 2009), reveals a fundamental role for RhoG in phagocytosis by different receptors. Taken together with our data, a pattern emerges for the key participation of RhoG in FccR-and CR3-mediated internalisation, as well as downstream of other phagocytic receptors.…”

Section: Resultsmentioning

confidence: 99%

RhoG is required for both FcγR- and CR3-mediated phagocytosis

Tzircotis

Braga

Caron

2011

Journal of Cell Science

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SummaryPhagocytosis is a highly ordered process orchestrated by signalling through Rho GTPases to locally organise the actin cytoskeleton and drive particle uptake. Specific Rho family members that regulate phagocytosis are not known, as the majority of studies have relied on the use of dominant-negative mutants and/or toxins, which can inactivate multiple Rho GTPases. To identify the relevant GTPases for phagocytosis through the Fcc receptor (FccR) and complement receptor 3 (CR3), we depleted 20 Rho proteins individually in an RNA interference (RNAi) screen. We find that distinct GTPase subsets are required for actin polymerisation and uptake by macrophages: FccR-dependent engulfment requires Cdc42 and Rac2 (but not Rac1), whereas CR3 requires RhoA. Surprisingly, RhoG is required for particle uptake through both FccR and CR3. RhoG has been previously linked to Rac and Cdc42 signalling in different model systems, but not to RhoA. Interestingly, we find that RhoG is also recruited and activated at phagocytic cups downstream of FccR and CR3, irrespective of their distinct actin structures and mechanisms of internalisation. Thus, the functional links between RhoG and RhoA downstream of CR3-dependent phagocytosis are new and unexpected. Our data suggest a broad role for RhoG in consolidating signals from multiple receptors during phagocytosis.

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Acting on Actin: Rac and Rho Played by Yersinia

Aepfelbacher

Wolters

2016

Current Topics in Microbiology and Immunology

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Pathogenic bacteria of the genus Yersinia include Y. pestis-the agent of plaque-and two enteropathogens, Y. enterocolitica, and Y. pseudotuberculosis. These pathogens have developed an array of virulence factors aimed at manipulating Rho GTP-binding proteins and the actin cytoskeleton in host cells to cross the intestinal barrier and suppress the immune system. Yersinia virulence factors include outer membrane proteins triggering cell invasion by binding to integrins, effector proteins injected into host cells to manipulate Rho protein functions and a Rho protein-activating exotoxin. Here, we present an overview of how Yersinia and host factors are integrated in a regulatory network that orchestrates the subversion of host defense.

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Yersinia enterocolitica differentially modulates RhoG activity in host cells

Cited by 34 publications

References 55 publications

Yersinia pseudotuberculosisVirulence Determinants Invasin, YopE, and YopT Modulate RhoG Activity and Localization

Yersinia pseudotuberculosisVirulence Determinants Invasin, YopE, and YopT Modulate RhoG Activity and Localization

RhoG is required for both FcγR- and CR3-mediated phagocytosis

Acting on Actin: Rac and Rho Played by Yersinia

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