The<i>Legionella</i>-driven PtdIns(4)<i>P</i>gradient at LCV-ER membrane contact sites promotes Vap-, OSBP- and Sac1-dependent pathogen vacuole remodeling

Vormittag, Simone; Hüsler, Dario; Haneburger, Ina; Kroninger, Tobias; Anand, Aby; Prantl, Manuel; Barisch, Caroline; Maaß, Sandra; Becher, Dörte; Letourneur, François; Hilbi, Hubert

doi:10.1101/2022.06.17.496549

Cited by 2 publications

(3 citation statements)

References 90 publications

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“…The increased appreciation of interorganelle interactions in recent years has unveiled a variety of MCSs in eukaryotes 39 . These closely apposed and tethered membranes facilitate numerous cellular processes, making them prime candidates for microbial control or mimicry 9,10 . Thus far, examples of pathogenic subversion of MCSs have been limited to interactions between eukaryotic membrane compartments [4][5][6] .…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

An obligate intracellular bacterial pathogen forms a direct, interkingdom membrane contact site

Acevedo-Sánchez

Woida

Kräemer

et al. 2023

Preprint

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Interorganelle communication regulates cellular homeostasis through the formation of tightly-associated membrane contact sites 1,3. Prior work has identified several ways that intracellular pathogens alter contacts between eukaryotic membranes 4,6, but there is no existing evidence for contact sites spanning eukaryotic and prokaryotic membranes. Here, using a combination of live-cell microscopy and transmission and focused-ion-beam scanning electron microscopy, we demonstrate that the intracellular bacterial pathogenRickettsia parkeriforms a direct membrane contact site between its bacterial outer membrane and the rough endoplasmic reticulum (ER), with tethers that are approximately 55 nm apart. Depletion of the ER-specific tethers VAPA and VAPB reduced the frequency of rickettsia-ER contacts, suggesting these interactions mimic organelle-ER contacts. Overall, our findings illuminate a direct, interkingdom membrane contact site uniquely mediated by rickettsia that seems to mimic traditional host MCSs.

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Section: Discussionmentioning

confidence: 99%

“…Recent research indicates that ER-mediated MCSs are susceptible to pathogen subversion 9,10 . Pathogens appear to either manipulate pre-existing MCSs 4 or establish new ones between the ER and the host-derived membrane that harbors the pathogen 6 .…”

Section: Introductionmentioning

confidence: 99%

An obligate intracellular bacterial pathogen forms a direct, interkingdom membrane contact site

Acevedo-Sánchez

Woida

Kräemer

et al. 2023

Preprint

View full text Add to dashboard Cite

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“…Recent research has highlighted the emerging roles of MCS in mammalian innate immunity 12 . Moreover, pathogens have developed strategies to target and subvert MCS, perturbing interorganelle communications to undermine host immune defenses and exploit cellular resources 13,14 . However, the involvement of MCS in plant-pathogen interactions remains unexplored.…”

Section: Introductionmentioning

confidence: 99%

Membrane Contact Sites Between Chloroplasts and Pathogen Interface Underpin Plant Focal Immune Responses

Savage

Erickson

Prautsch

et al. 2021

Preprint

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When a plant detects a pathogen, chloroplasts terminate photosynthetic activity and uptake vital roles in the immune system to help stave off infection, including the production of defense hormone precursors and antimicrobial reactive oxygen species. Additionally, chloroplasts associate with the nucleus and produce greater numbers of tubular extensions called stromules during immune challenge. We previously showed that during infection by the potato blight pathogen Phytophthora infestans, chloroplasts accumulate at the pathogen haustoria, hyphal extensions that are accommodated within the host cell. However, the extent to which chloroplast positioning around haustoria, or at the nucleus, contributes to immunity during infection remains unknown. Here we show a striking increase in the susceptibility to P. infestans of Nicotiana benthamiana CRISPR knock-out lines lacking the chloroplast movement and anchoring gene, CHLOROPLAST UNUSUAL POSITIONING 1 (CHUP1). However, the positioning of chloroplasts around the haustorium or nucleus is not impaired in the absence of CHUP1. Further, loss of CHUP1 leads to an extreme clustering of chloroplasts around the nucleus in the presence and absence of infection, showing that greater chloroplast-nucleus association does not necessarily equate to more robust immunity. While plants lacking CHUP1 have reduced basal stromules, they are still able to induce stromules following immune stimulation, indicating that multiple populations of stromules exist. Lastly, we found that CHUP1 is required for proper deposition of callose - a cell wall material implicated in pathogen penetration resistance - around P. infestans haustorium, but not for other core immune processes. Our results implicate chloroplasts in plant focal immunity and point to a key role of CHUP1 in facilitating the deposition of defense material at the pathogen interface.

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TheLegionella-driven PtdIns(4)Pgradient at LCV-ER membrane contact sites promotes Vap-, OSBP- and Sac1-dependent pathogen vacuole remodeling

Cited by 2 publications

References 90 publications

An obligate intracellular bacterial pathogen forms a direct, interkingdom membrane contact site

An obligate intracellular bacterial pathogen forms a direct, interkingdom membrane contact site

Membrane Contact Sites Between Chloroplasts and Pathogen Interface Underpin Plant Focal Immune Responses

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