Blebology: principles of bleb-based migration

García-Arcos, Juan Manuel; Jha, Ankita; Waterman, Clare M.; Piel, Matthieu

doi:10.1016/j.tcb.2024.02.009

Cited by 7 publications

(4 citation statements)

References 121 publications

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“…85,86 Cells were confined for over an hour to ensure the predominance of the leader bleb phenotype (Figure 5A). 87 Our findings indicated that Flipper-TR lifetime gradients are absent at the protruding front of leader bleb migrating cells (Figures 5B and 5C). The lifetime was only marginally increased at the rear of the leader bleb, adjacent to the uropod (i.e.…”

Section: Substrate Rigidity and Adhesiveness Modulate Membrane Tensionmentioning

confidence: 52%

“…Therefore, contrary to what has been suggested, 35 the existence of tension gradients does not depend on the cell type, but on the migration mode. 87 At the ventral membrane, attached to the coverslip, we find strong inhomogeneities, which disappear at the apical membrane not attached to the substrate (Figure 5G, top panel). This allows us to propose a mechanism by which membrane tension gradients can be sustained in adherent cells (Figure 5G).…”

Section: Discussionmentioning

confidence: 86%

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Actin dynamics sustains spatial gradients of membrane tension in adherent cells

García-Arcos,

Mehidi,

Velázquez

et al. 2024

Preprint

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Tension propagates in lipid bilayers over hundreds of microns within milliseconds, precluding the formation of tension gradients. Nevertheless, plasma membrane tension gradients have been evidenced in migrating cells and along axons. Here, using a fluorescent membrane tension probe, we show that membrane tension gradients exist in all adherent cells, whether they migrate or not. Non-adhering cells do not display tension gradients. We further show that branched actin increases tension, while membrane-to-cortex attachments facilitate its propagation. Tension is the lowest at the edge of adhesion sites and highest at protrusions, setting the boundaries of the tension gradients. By providing a quantitative and mechanistic basis behind the organization of membrane tension gradients, our work explains how they are actively sustained in adherent cells.

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Section: Substrate Rigidity and Adhesiveness Modulate Membrane Tensionmentioning

confidence: 52%

Section: Discussionmentioning

confidence: 86%

Actin dynamics sustains spatial gradients of membrane tension in adherent cells

García-Arcos,

Mehidi,

Velázquez

et al. 2024

Preprint

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“…3b) and even occasionally cells with a blebbing cell front during migration, both indicators of a high degree of intracellular contractility. This finding was surprising, as DCs have not yet been described to employ a blebbing-like migration mode, which is used by some cell types for forward movement 24,25 . As DCs typically have cell fronts composed of highly dynamic veil-like protrusions, this finding indicated a shift in the balance of cellular progressiveness and contractility 26 upon parasite infection.…”

Section: Resultsmentioning

confidence: 98%

Hijacked Immune Cells Traverse Microenvironmental Barriers by Positioning and Pushing their Intracellular Parasite Cargo

Ruiz-Fernandez,

Jiang,

Mortazavi

et al. 2024

Preprint

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Intracellular pathogens hijack the cytoskeletal networks of their host cells to facilitate their uptake, drive their intracellular motility, or prevent their degradation. While many underlying principles have been explored during host cell infections by intracellular bacteria like Listeria, Chlamydia, or Shigella, it remains less well understood how large eukaryotic intracellular parasites like Toxoplasma gondii exploit the host cytoskeleton. In particular, how Toxoplasma achieves its transport within highly motile immune cells remains largely unknown despite its large intracellular size. Here, we discover that Toxoplasma gondii hijacks host myosin forces for translocation through microenvironmental barriers along immune cell migration paths. Using highly defined micro-engineered migration paths and dendritic cells as a highly motile immune cell model, we reveal that large parasitic cargos acquire a surprising intracellular position frontward of the host nucleus and microtubule-organizing center. This frontward localization of parasitic cargos depends on microenvironmental confinement and host myosin activity. We identify that the parasite cargos cause high contractility within their motile host cells mediated by host myosin-II, thereby facilitating their squeezing and deformation to enable transversal through confining microenvironments. Our findings establish parasitic hijacking of myosin forces as a novel principle of how parasites exploit host cytoskeletal networks.

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“…This study aimed to reveal the role of fluctuating dynamics in the cytoplasm on motor-driven transport in vivo, focusing on the effects of actomyosin dynamics in the cytoplasm. Not only do actin and myosin networks produce contractile force in the cell cortex to induce the morphological dynamics of cells 41,42 , but they also form networks in the cytoplasm [43][44][45][46] . These cytoplasmic actin or actomyosin networks not only facilitate directed motion, such as the transport of the cell nucleus and chromosomes in mouse embryos [41][42][43][44][45] and starfish oocytes 47,48 , but also generate active random forces within the cytoplasm, consequently influencing the physical properties of the cytoplasm 33 .…”

Section: Introductionmentioning

confidence: 99%

Active fluctuations of cytoplasmic actomyosin networks facilitate dynein-driven intracellular transport along microtubules

Torisawa,

Saito,

Furuta

et al. 2024

Preprint

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Inside cells, molecular motors transport cargoes within the actively fluctuating environment known as the cytoplasm. How fluctuations in the cytoplasm affect motor-driven transport is not fully understood. In this study, we investigated the role of fluctuations for transport along microtubules usingC. elegansearly embryos, focusing on transport driven by cytoplasmic dynein. An artificial motor-cargo complex showed faster transportin vivothanin vitro, suggesting anin vivoacceleration mechanism. We also found that endogenous early endosome transport by dynein is significantly enhanced by the fluctuations in the cytoplasm, which is attributed to the activity of actomyosin networks. Anin vitroforce measurement of dynein suggests that the asymmetric force response would play a key role in the acceleration. This study provides insights into a regulatory mechanism of molecular motors within actively fluctuating cytoplasm, potentially utilizing random force originating from fluctuating dynamics in the cytoplasm to increase transport efficiency.

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Blebology: principles of bleb-based migration

Cited by 7 publications

References 121 publications

Actin dynamics sustains spatial gradients of membrane tension in adherent cells

Actin dynamics sustains spatial gradients of membrane tension in adherent cells

Hijacked Immune Cells Traverse Microenvironmental Barriers by Positioning and Pushing their Intracellular Parasite Cargo

Active fluctuations of cytoplasmic actomyosin networks facilitate dynein-driven intracellular transport along microtubules

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