Autophagy and Intracellular Membrane Trafficking Subversion by Pathogenic Yersinia Species

Lemarignier, Marion; Pizarro‐Cerdá, Javier

doi:10.3390/biom10121637

Cited by 10 publications

(9 citation statements)

References 59 publications

(87 reference statements)

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“…Both Yersinia and Listeria have been shown to activate autophagic mechanisms, and it was suggested that those mechanisms facilitate the destruction of the bacteria [44,45]. Activation of MLKL was also reported to facilitate autophagy [46].…”

Section: Mlkl Ubiquitination Also Facilitates the Destruction Of Some Other Intracellular Bacteriamentioning

confidence: 99%

Site-specific ubiquitination of MLKL targets it to endosomes and targets Listeria and Yersinia to the lysosomes

2022

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Phosphorylation of the pseudokinase mixed lineage kinase domain-like protein (MLKL) by the protein kinase RIPK3 targets MLKL to the cell membrane, where it triggers necroptotic cell death. We report that conjugation of K63-linked polyubiquitin chains to distinct lysine residues in the N-terminal HeLo domain of phosphorylated MLKL (facilitated by the ubiquitin ligase ITCH that binds MLKL via a WW domain) targets MLKL instead to endosomes. This results in the release of phosphorylated MLKL within extracellular vesicles. It also prompts enhanced endosomal trafficking of intracellular bacteria such as Listeria monocytogenes and Yersinia enterocolitica to the lysosomes, resulting in decreased bacterial yield. Thus, MLKL can be directed by specific covalent modifications to differing subcellular sites, whence it signals either for cell death or for non-deadly defense mechanisms.

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Section: Mlkl Ubiquitination Also Facilitates the Destruction Of Some Other Intracellular Bacteriamentioning

confidence: 99%

Site-specific ubiquitination of MLKL targets it to endosomes and targets Listeria and Yersinia to the lysosomes

2022

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“…If decoration by LC3B-positive membranes is only delayed to late time points of infection and if this also leads to lysosomal degradation of engulfed bacteria deserves further investigation. For several Yersinia strains it was reported that degradation by fusion with lysosomes is inhibited and Yersinia is able to replicate in a non-acidic autophagosome (Connor et al, 2018; Lemarignier & Pizarro-Cerda, 2020; Moreau et al, 2010; Straley & Harmon, 1984). Further investigations assessing acidification of LC3B-positive compartments and interfering with autophagosome formation using Lysotracker, siRNA approaches, and autophagy inhibitors such as 3-MA in combination with replication assays could help to understand the host-pathogen interactions in SPA in more detail.…”

Section: Discussionmentioning

confidence: 99%

From vacuole to cytosol – Disruptive invasion triggers cytosolic release ofSalmonellaParatyphi A and subsequent cytosolic motility favors evasion of xenophagy

Scharte

Franzkoch

Hensel

2022

Preprint

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Salmonella enterica is a common foodborne, facultative intracellular enteropathogen. Typhoidal S. enterica serovars like Paratyphi A (SPA) are human restricted and cause a severe systemic disease, while many S. enterica serovars like Typhimurium (STM) have broad host range, and in human hosts usually lead to self-limiting gastroenteritis. There are key differences between typhoidal and non-typhoidal Salmonella in pathogenesis, but underlying mechanisms remain largely unknown. Several genes encoding Salmonella pathogenicity island (SPI) effector proteins are absent or pseudogenes in SPA. Expression of virulence and metabolism genes show differential expression compared to STM. The intracellular transcriptomic architecture and phenotypes during presence in epithelial cells were recently described. Surprisingly, induction of motility, flagella and chemotaxis genes showed distinct expression patterns in intracellular SPA vs. STM and led to cytosolic motility of SPA. This study applies single cell microscopic analyses approaches to investigate the triggers and cellular consequences of cytosolic motility. Live cell imaging (LCI) revealed that SPA invades host cells in a highly cooperative manner. Extensive membrane ruffling at the invasion site leads to increased membrane damage in the nascent SCV with subsequent cytosolic release. After release into the cytosol, motile bacteria showed same velocity as under culture conditions used for infection. Reduced capture of SPA by autophagosomal membranes was observed by LCI and electron microscopy. Our results reveal flagella-mediated cytosolic motility as possible xenophagy evasion mechanism that could drive disease progression and contributes to dissemination of invasion-primed SPA during systemic infection.

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“…Although macrophages are important phagocytic cells that have the ability to kill bacteria, there is evidence that Y. ruckeri survives and multiplies intracellularly in these cells (Ryckaert et al, 2010;Welch & Wiens, 2005). Other pathogenic Yersinia species, such as Y. enterocolitica and Y pseudotuberculosis, have been shown to survive in macrophages (Lemarignier & Pizarro-Cerda, 2020). Similarly to Y. ruckeri, these human pathogens invade through the intestine before spreading to other tissues.…”

Section: Discussionmentioning

confidence: 99%

Tissue‐specific differences in detection of Yersinia ruckeri carrier status in rainbow trout (Oncorhynchus mykiss)

Sibinga

Marquis

2021

Journal of Fish Diseases

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Effective monitoring for subclinical infections is a cornerstone of proactive disease management in aquaculture. Salmonid fish that survive enteric redmouth disease (ERM) can carry Yersinia ruckeri as a latent infection for several months, potentially facilitating cryptic spread between facilities that exchange fish. In this study, fingerling rainbow trout (Oncorhynchus mykiss) were infected by immersion and sampled for up to 14 weeks post-infection. Yersinia ruckeri was cultured from the posterior kidney of more than 89% of fish up to 4 weeks post-infection, but from 2% or fewer of fish sampled at later time points. In contrast, qPCR-based detection of the Y. ruckeri 16s rRNA gene in intestine and spleen extracts revealed a much higher rate of infection: at 14 weeks post-infection Y. ruckeri was detected in nearly 50% of spleens and 15% of intestines. The difference between spleen and intestine is likely due at least in part to technical limitations of qPCR on intestinal DNA extracts; accordingly, we propose that qPCR of spleen DNA ought to be considered the preferred standard for detection of carriers of Y. ruckeri.

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Autophagy and Intracellular Membrane Trafficking Subversion by Pathogenic Yersinia Species

Cited by 10 publications

References 59 publications

Site-specific ubiquitination of MLKL targets it to endosomes and targets Listeria and Yersinia to the lysosomes

Site-specific ubiquitination of MLKL targets it to endosomes and targets Listeria and Yersinia to the lysosomes

From vacuole to cytosol – Disruptive invasion triggers cytosolic release ofSalmonellaParatyphi A and subsequent cytosolic motility favors evasion of xenophagy

Tissue‐specific differences in detection of Yersinia ruckeri carrier status in rainbow trout (Oncorhynchus mykiss)

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