The Second Type VI Secretion System of Pseudomonas aeruginosa Strain PAO1 Is Regulated by Quorum Sensing and Fur and Modulates Internalization in Epithelial Cells

Sana, Thibault G.; Hachani, Abderrahman; Bucior, Iwona; Soscia, Chantal; Garvis, Steve; Termine, Elise; Engel, Joanne N.; Filloux, Alain; Bleves, Sophie

doi:10.1074/jbc.m112.376368

Cited by 186 publications

(247 citation statements)

References 76 publications

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“…The expression of a type-III secretion system (T3SS) by P. aeruginosa and T3SS-and T6SS-secreted effector proteins have been reported to be required for the cellular invasion and are supposed to influence the growthphase dependent cellular uptake of P. aeruginosa (11,(42)(43)(44)(45). However, our data suggest that initial membrane curvature and wrapping of the bacterium by the host PM depends neither on a bacterial secretion system nor on secreted effector proteins.…”

Section: Discussioncontrasting

confidence: 53%

A lipid zipper triggers bacterial invasion

Eierhoff

Bastian

Thuenauer

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

125

161

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Significance Entry of bacteria into host cells critically depends on their proper engulfment by the plasma membrane. So far, actin polymerization has been described as a major driving force in this process. However, our study reveals that the interaction of the bacterial surface lectin LecA with the host cell glycosphingolipid Gb3 is fully sufficient to promote engulfment of Pseudomonas aeruginosa , whereas actin polymerization is dispensable. Hence, the formation of a “lipid zipper” represents a previously unidentified mechanism of bacterial uptake and demonstrates that bacterial pathogens have evolved lipid-based invasion strategies that may function in addition to protein receptor-based ones. Furthermore, by identifying the LecA/Gb3 interaction as the major invasion-promoting factor, our study provides new targets for drugs that may prevent bacterial invasion and dissemination.

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Section: Discussioncontrasting

confidence: 53%

A lipid zipper triggers bacterial invasion

Eierhoff

Bastian

Thuenauer

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

125

161

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“…A multicomponent signaling cascade, TagQRSTPpkA-PppA-Fha1, is required for the precise retaliatory response that activates the firing of H1-T6SS at the exact site of external assault (34,38). Although the H2-T6SS and the H3-T6SS clusters are implicated in both antimicrobial and antieukaryote activities (26,39,40), their contribution to bacterial killing is substantially less effective than that of the H1-T6SS, as exhibited by prey cell tolerance of the P. aeruginosa mutant lacking the H1-T6SS (25,38).…”

Section: Ystic Fibrosis (Cf) Is a Common Lethal Inherited Disease Inmentioning

confidence: 99%

Chelation of Membrane-Bound Cations by Extracellular DNA Activates the Type VI Secretion System in Pseudomonas aeruginosa

et al. 2016

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e Pseudomonas aeruginosa employs its type VI secretion system (T6SS) as a highly effective and tightly regulated weapon to deliver toxic molecules to target cells. T6SS-secreted proteins of P. aeruginosa can be detected in the sputum of cystic fibrosis (CF) patients, who typically present a chronic and polymicrobial lung infection. However, the mechanism of T6SS activation in the CF lung is not fully understood. Here we demonstrate that extracellular DNA (eDNA), abundant within the CF airways, stimulates the dynamics of the H1-T6SS cluster apparatus in Pseudomonas aeruginosa PAO1. Addition of Mg 2؉ or DNase with eDNA abolished such activation, while treatment with EDTA mimicked the eDNA effect, suggesting that the eDNA-mediated effect is due to chelation of outer membrane-bound cations. DNA-activated H1-T6SS enables P. aeruginosa to nonselectively attack neighboring species regardless of whether or not it was provoked. Because of the importance of the T6SS in interspecies interactions and the prevalence of eDNA in the environments that P. aeruginosa inhabits, our report reveals an important adaptation strategy that likely contributes to the competitive fitness of P. aeruginosa in polymicrobial communities.

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“…T6SSs are versatile systems that deliver toxins into either eukaryotic or prokaryotic cells, or both (10). For example, the Vibrio cholerae Vas and the Pseudomonas aeruginosa H2-T6SS target and kill bacteria but also inject toxins into host cells to prevent phagocytosis or to facilitate invasion, respectively (13)(14)(15)(16)(17)(18). The T6SS is a multiprotein machine that uses a contractile mechanism for toxin secretion (19).…”

mentioning

confidence: 99%

Salmonella Typhimurium utilizes a T6SS-mediated antibacterial weapon to establish in the host gut

Sana

Flaugnatti

Lugo

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

287

292

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The mammalian gastrointestinal tract is colonized by a high-density polymicrobial community where bacteria compete for niches and resources. One key competition strategy includes cell contact-dependent mechanisms of interbacterial antagonism, such as the type VI secretion system (T6SS), a multiprotein needle-like apparatus that injects effector proteins into prokaryotic and/or eukaryotic target cells. However, the contribution of T6SS antibacterial activity during pathogen invasion of the gut has not been demonstrated. We report that successful establishment in the gut by the enteropathogenic bacterium Salmonella enterica serovar Typhimurium requires a T6SS encoded within Salmonella pathogenicity island-6 (SPI-6). In an in vitro setting, we demonstrate that bile salts increase SPI-6 antibacterial activity and that S. Typhimurium kills commensal bacteria in a T6SS-dependent manner. Furthermore, we provide evidence that one of the two T6SS nanotube subunits, Hcp1, is required for killing Klebsiella oxytoca in vitro and that this activity is mediated by the specific interaction of Hcp1 with the antibacterial amidase Tae4. Finally, we show that K. oxytoca is killed in the host gut in an Hcp1-dependent manner and that the T6SS antibacterial activity is essential for Salmonella to establish infection within the host gut. Our findings provide an example of pathogen T6SS-dependent killing of commensal bacteria as a mechanism to successfully colonize the host gut.

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The Second Type VI Secretion System of Pseudomonas aeruginosa Strain PAO1 Is Regulated by Quorum Sensing and Fur and Modulates Internalization in Epithelial Cells

Cited by 186 publications

References 76 publications

A lipid zipper triggers bacterial invasion

A lipid zipper triggers bacterial invasion

Chelation of Membrane-Bound Cations by Extracellular DNA Activates the Type VI Secretion System in Pseudomonas aeruginosa

Salmonella Typhimurium utilizes a T6SS-mediated antibacterial weapon to establish in the host gut

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