Vesicle trafficking pathways that direct cell migration in 3D matrices and in vivo

Wilson, Beverley; Allen, Jennifer L.; Caswell, Patrick T.

doi:10.1111/tra.12605

Cited by 40 publications

(46 citation statements)

References 111 publications

(136 reference statements)

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“…Similarly to internalisation, intracellular sorting of integrins is fine-tuned by other receptors and ECM ligands and this process impinges on efficient cell migration 14,20 . For example, the tyrosine phosphorylation status of Syndecan-4 acts as a switch controlling differential recycling of αvβ3- and α5β1-integrins, and the tightly balanced availability of these two receptors at the plasma membrane determines FA half-life and cell migration behaviour 50 .…”

Section: Integrin Endocytic Trafficking Pathwaysmentioning

confidence: 99%

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Integrin trafficking in cells and tissues

et al. 2019

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Cell adhesion to the extracellular matrix (ECM) is fundamental to metazoan multicellularity and is accomplished primarily through the integrin family of cell-surface receptors. Integrins are internalised and enter the endo/exocytic pathway before being recycled back to the plasma membrane. The trafficking of this extensive protein family is regulated in multiple context-dependent ways to modulate integrin function in the cell. Here we discuss recent advances in understanding the mechanisms and cellular roles of integrin endocytic trafficking.

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Section: Integrin Endocytic Trafficking Pathwaysmentioning

confidence: 99%

“…2a). Endocytosed integrins are also able to transmit intracytoplasmic “inside-in” signals either through recruitment of focal adhesion kinase (FAK), and possibly other effectors 16,17 , or by enhancing the signalling of co-trafficking growth factor receptors 18–20 (Fig. 1b).…”

Section: Introductionmentioning

confidence: 99%

Integrin trafficking in cells and tissues

et al. 2019

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“…These data point to a relevant role for TUBB in postendocytic transport; interestingly, the expression level of TUBB5 was found to be upregulated during the endocytosis-mediated invasion of S. agalactiae in H9C2 cells [36], and Jeon and colleagues, using a cell sorting-based functional selection of phagocytosis promoting genes, identified TUBB5 as one of the genes conferring phagocytic activity to mouse fibroblasts [37]. Moreover, vesicle trafficking, controlling the availability and spatial distribution of cargoes, influences the movement of cells [38,39], and the impairment in EGF signaling perturbs the migration of pancreatic islet cells and keratinocytes in EGF-receptor deficient mice [40,41].…”

Section: Discussionmentioning

confidence: 99%

TUBB Variants Underlying Different Phenotypes Result in Altered Vesicle Trafficking and Microtubule Dynamics

Sferra

Petrini

Bellacchio

et al. 2020

IJMS

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Tubulinopathies are rare neurological disorders caused by alterations in tubulin structure and function, giving rise to a wide range of brain abnormalities involving neuronal proliferation, migration, differentiation and axon guidance. TUBB is one of the ten β-tubulin encoding genes present in the human genome and is broadly expressed in the developing central nervous system and the skin. Mutations in TUBB are responsible for two distinct pathological conditions: the first is characterized by microcephaly and complex structural brain malformations and the second, also known as “circumferential skin creases Kunze type” (CSC-KT), is associated to neurological features, excess skin folding and growth retardation. We used a combination of immunocytochemical and cellular approaches to explore, on patients’ derived fibroblasts, the functional consequences of two TUBB variants: the novel mutation (p.N52S), associated with basal ganglia and cerebellar dysgenesis, and the previously reported variant (p.M73T), linked to microcephaly, corpus callosum agenesis and CSC-KT skin phenotype. Our results demonstrate that these variants impair microtubule (MT) function and dynamics. Most importantly, our studies show an altered epidermal growth factor (EGF) and transferrin (Tf) intracellular vesicle trafficking in both patients’ fibroblasts, suggesting a specific role of TUBB in MT-dependent vesicular transport.

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“…Importantly, retrograde membrane flow is implicated in many different motility modes of eukaryotic cells and recent evidence demonstrates important roles for membrane trafficking in the regulation of cell migration in a variety of contexts. For example, one critical role of an endocytic-secretory cycle is the internalisation and recycling of adhesion receptors, such as integrins or syndecans (50). Another critical role is the maintenance of a constant cell surface (51,52).…”

Section: A Link Between Gliding Motility Retrograde Membrane Flow Smentioning

confidence: 99%

Apicomplexan motility depends on the operation of an endocytic-secretory cycle

Gras

Jiménez-Ruiz

et al. 2018

Preprint

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Apicomplexan parasites invade host cells in an active process, involving their ability to move by gliding motility and invasion. While the acto-myosin-system of the parasite plays a crucial role in the formation and release of attachment sites during this process, there are still open questions, such as how the force powering motility is generated. In many eukaryotes a secretory-endocytic cycle leads to recycling of receptors (integrins), necessary to form attachment sites, regulation of surface area during motility and generation of retrograde membrane flow. Here we demonstrate that endocytosis operates during gliding motility in Toxoplasma gondii and appears to be crucial for the establishment of retrograde membrane flow, since inhibition of endocytosis blocks retrograde flow and motility. We identified lysophosphatidic acid (LPA) as a potent stimulator of endocytosis and demonstrate that extracellular parasites can efficiently incorporate exogenous material, such as nanogold particles.Furthermore, we show that surface proteins of the parasite are recycled during this process.Interestingly, the endocytic and secretory pathways of the parasite converge, and endocytosed material is subsequently secreted, demonstrating the operation of an endocytic-secretory cycle.Together our data consolidate previous findings and we propose a novel model that reconciles parasite motility with observations in other eukaryotes: the fountain-flow-model for apicomplexan parasite motility. Abbreviation: LPA Lysophosphatidic acid, CDE clathrin-dependant endocytosis, CDI clathrinindependent endocytosis, CD Cytochalasin-D, TFDC Trifluoperazine di-hydrochloride, DN Dominant negative, CHC clathrin heavy chain, LPC Lysophosphatidyl choline, BP Bodipy, NGP nanogold particles, VAC vacuolar-like compartment, ER endoplasmic reticulum, CLEM corelative light and electron microscopy, TEM transmission electron microscopy. (University of Geneva), Prof. Vern Carruthers (University of Michigan), and Dr Maryse Lebrun (University of Montpellier) for generously providing antibodies and parasite strains.

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Vesicle trafficking pathways that direct cell migration in 3D matrices and in vivo

Cited by 40 publications

References 111 publications

Integrin trafficking in cells and tissues

Integrin trafficking in cells and tissues

TUBB Variants Underlying Different Phenotypes Result in Altered Vesicle Trafficking and Microtubule Dynamics

Apicomplexan motility depends on the operation of an endocytic-secretory cycle

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