Cdc42 localization and cell polarity depend on membrane traffic

Osmani, Naël; Péglion, Florent; Chavrier, Philippe; Etienne-Manneville, Sandrine

doi:10.1083/jcb.201003091

Cited by 162 publications

(173 citation statements)

References 53 publications

Supporting

Mentioning

160

Contrasting

Order By: Relevance

“…Like for Rac, its activation needs to be spatially restricted to the leading edge to promote directed migration. In a wound-induced astrocyte migration assay dynamic Cdc42 positive vesicles were observed to move in a directed manner towards the leading edge [44]. Again Arf6 served as decisive factor for vesicular transport of Cdc42 and its GEF bPIX to the leading edge [44] reinforcing the notion that Arf6 controls crucial membrane transport steps in directed cell migration.…”

Section: Regulating Downstream Signaling and Actin Regulatory Componentsmentioning

confidence: 78%

On the move: endocytic trafficking in cell migration

Maritzen

Schachtner

Legler

2015

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

Directed cell migration is a fundamental process underlying diverse physiological and pathophysiological phenomena ranging from wound healing and induction of immune responses to cancer metastasis. Recent advances reveal that endocytic trafficking contributes to cell migration in multiple ways. (1) At the level of chemokines and chemokine receptors: internalization of chemokines by scavenger receptors is essential for shaping chemotactic gradients in tissue, whereas endocytosis of chemokine receptors and their subsequent recycling is key for maintaining a high responsiveness of migrating cells. (2) At the level of integrin trafficking and focal adhesion dynamics: endosomal pathways do not only modulate adhesion by delivering integrins to their site of action, but also by supplying factors for focal adhesion disassembly. (3) At the level of extracellular matrix reorganization: endosomal transport contributes to tumor cell migration not only by targeting integrins to invadosomes but also by delivering membrane type 1 matrix metalloprotease to the leading edge facilitating proteolysis-dependent chemotaxis. Consequently, numerous endocytic and endosomal factors have been shown to modulate cell migration. In fact key modulators of endocytic trafficking turn out to be also key regulators of cell migration. This review will highlight the recent progress in unraveling the contribution of cellular trafficking pathways to cell migration.

show abstract

Section: Regulating Downstream Signaling and Actin Regulatory Componentsmentioning

confidence: 78%

On the move: endocytic trafficking in cell migration

Maritzen

Schachtner

Legler

2015

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

show abstract

“…The evolutionary conserved proteins localize asymmetrically before morphological polarization and mutually antagonize each other 5 . The maintenance of cell polarity is a highly dynamic process as interference with vesicle trafficking proteins such as Rab8 and Rab11 results in loss of already established cellular asymmetry [6][7][8] .…”

mentioning

confidence: 99%

AmotL2 disrupts apical–basal cell polarity and promotes tumour invasion

et al. 2014

View full text Add to dashboard Cite

The establishment and maintenance of apical-basal cell polarity is essential for the functionality of glandular epithelia. Cell polarity is often lost in advanced tumours correlating with acquisition of invasive and malignant properties. Despite extensive knowledge regarding the formation and maintenance of polarity, the mechanisms that deregulate polarity in metastasizing cells remain to be fully characterized. Here we show that AmotL2 expression correlates with loss of tissue architecture in tumours from human breast and colon cancer patients. We further show that hypoxic stress results in activation of c-Fos-dependent expression of AmotL2 leading to loss of polarity. c-Fos/hypoxia-induced p60 AmotL2 interacts with the Crb3 and Par3 polarity complexes retaining them in large vesicles and preventing them from reaching the apical membrane. The resulting loss of polarity potentiates the response to invasive cues in vitro and in vivo in mice. These data provide a molecular mechanism how hypoxic stress deregulates cell polarity during tumour progression.

show abstract

“…Rac1 regulates actin dynamics and ruffle formation at the leading edge of migrating cells and its activity is essential for cell adhesion and migration. TIAM-1-mediated activation of Rac1 on endosomes and subsequent polarized transport to the plasma membrane has been proposed as a way to restrict Rac activity to sites of membrane protrusion [11,12]. In line with this model, Sandri et al show that active R-Ras and RIN2 colocalize with Rac1 on endosomes and that the endosomal Rac GEF TIAM-1 is necessary for R-Ras-and RIN2-induced cell adhesion.…”

mentioning

confidence: 52%

A tale of three GTPases and a RIN in endothelial cell adhesion

Fernandez‐Borja

2012

Cell Res

View full text Add to dashboard Cite

Endothelial cell adhesion to the extracellular matrix regulates migration and outgrowth of blood vessels during angiogenesis. Cell adhesion is mediated by integrins, which transduce signals from the extracellular environment into the cell and, in turn, are regulated by intracellular signaling molecules. In a paper recently published in Cell Research, Sandri et al. show that RIN2 connects three GTPases, R-Ras, Rab5 and Rac1, to promote endothelial cell adhesion through the regulation of integrin internalization and Rac1 activation.

show abstract

Cdc42 localization and cell polarity depend on membrane traffic

Abstract: Arf6-dependent membrane dynamics concentrates active Cdc42 at the leading edge of migrating cells.

Cited by 162 publications

References 53 publications

On the move: endocytic trafficking in cell migration

On the move: endocytic trafficking in cell migration

AmotL2 disrupts apical–basal cell polarity and promotes tumour invasion

A tale of three GTPases and a RIN in endothelial cell adhesion

Contact Info

Product

Resources

About