scholarly journals Polarity sets the stage for cytokinesis

2012 ◽  
Vol 23 (1) ◽  
pp. 7-11 ◽  
Author(s):  
Heidi Hehnly ◽  
Stephen Doxsey
Keyword(s):  
Cell Migration ◽  
Cell Division ◽  
Cell Polarity ◽  
Membrane Trafficking ◽  
Cell Separation ◽  
Cell Polarization ◽  
Separation Step ◽  
Canonical Pathways

Cell polarity is important for a number of processes, from chemotaxis to embryogenesis. Recent studies suggest a new role for polarity in the orchestration of events during the final cell separation step of cell division called abscission. Abscission shares several features with cell polarization, including rearrangement of phosphatidylinositols, reorganization of microtubules, and trafficking of exocyst-associated membranes. Here we focus on how the canonical pathways for cell polarization and cell migration may play a role in spatiotemporal membrane trafficking events required for the final stages of cytokinesis.

scholarly journals Cdc42 localization and cell polarity depend on membrane traffic

2010 ◽  
Vol 191 (7) ◽  
pp. 1261-1269 ◽  
Author(s):  
Naël Osmani ◽  
Florent Peglion ◽  
Philippe Chavrier ◽  
Sandrine Etienne-Manneville
Keyword(s):  
Cell Migration ◽  
Cell Polarity ◽  
Membrane Trafficking ◽  
Membrane Traffic ◽  
Leading Edge ◽  
Cell Polarization ◽  
Membrane Dynamics ◽  
Cell Functions ◽  
Directed Cell Migration ◽  
Division Cell

Cell polarity is essential for cell division, cell differentiation, and most differentiated cell functions including cell migration. The small G protein Cdc42 controls cell polarity in a wide variety of cellular contexts. Although restricted localization of active Cdc42 seems to be important for its distinct functions, mechanisms responsible for the concentration of active Cdc42 at precise cortical sites are not fully understood. In this study, we show that during directed cell migration, Cdc42 accumulation at the cell leading edge relies on membrane traffic. Cdc42 and its exchange factor βPIX localize to intracytosplasmic vesicles. Inhibition of Arf6-dependent membrane trafficking alters the dynamics of Cdc42-positive vesicles and abolishes the polarized recruitment of Cdc42 and βPIX to the leading edge. Furthermore, we show that Arf6-dependent membrane dynamics is also required for polarized recruitment of Rac and the Par6–aPKC polarity complex and for cell polarization. Our results demonstrate influence of membrane dynamics on the localization and activation of Cdc42 and consequently on directed cell migration.

Atypical Rho GTPases RhoD and Rif integrate cytoskeletal dynamics and membrane trafficking

2014 ◽  
Vol 395 (5) ◽  
pp. 477-484 ◽  
Author(s):  
Pontus Aspenström
Keyword(s):  
Cell Migration ◽  
Cell Division ◽  
Membrane Trafficking ◽  
Rho Gtpases ◽  
Intracellular Transport ◽  
Cell Contraction ◽  
Cell Behaviour ◽  
Master Regulators ◽  
Cellular Processes ◽  
Cytoskeletal Dynamics

Abstract The Rho GTPases are essential regulators of basic cellular processes, including cell migration, cell contraction and cell division. Most studies still involve just the three canonical members, RhoA, Rac1 and Cdc42, although the Rho GTPases comprise at least 20 members. The aim of this review is to highlight some of the recent advances in our knowledge regarding the less-studied Rho members, with the focus on RhoD and Rif. The phenotypic alterations to cell behaviour that are triggered by RhoD and Rif suggest that they have unique impacts on cytoskeletal dynamics that distinguish them from the well-studied members of the Rho GTPases. In addition, RhoD has a role in the regulation of intracellular transport of vesicles. Taken together, the available data indicate that RhoD and Rif have functions as master regulators in the integration of cytoskeletal reorganisation and membrane trafficking.

scholarly journals P-cadherin promotes collective cell migration via a Cdc42-mediated increase in mechanical forces

2016 ◽  
Vol 212 (2) ◽  
pp. 199-217 ◽  
Author(s):  
Cédric Plutoni ◽  
Elsa Bazellieres ◽  
Maïlys Le Borgne-Rochet ◽  
Franck Comunale ◽  
Agusti Brugues ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cell Polarity ◽  
Cell Biology ◽  
Cell Polarization ◽  
Collective Cell Migration ◽  
Mechanical Forces ◽  
Tumor Aggressiveness ◽  
And Migration ◽  
Cell Cell

Collective cell migration (CCM) is essential for organism development, wound healing, and metastatic transition, the primary cause of cancer-related death, and it involves cell–cell adhesion molecules of the cadherin family. Increased P-cadherin expression levels are correlated with tumor aggressiveness in carcinoma and aggressive sarcoma; however, how P-cadherin promotes tumor malignancy remains unknown. Here, using integrated cell biology and biophysical approaches, we determined that P-cadherin specifically induces polarization and CCM through an increase in the strength and anisotropy of mechanical forces. We show that this mechanical regulation is mediated by the P-cadherin/β-PIX/Cdc42 axis; P-cadherin specifically activates Cdc42 through β-PIX, which is specifically recruited at cell–cell contacts upon CCM. This mechanism of cell polarization and migration is absent in cells expressing E- or R-cadherin. Thus, we identify a specific role of P-cadherin through β-PIX–mediated Cdc42 activation in the regulation of cell polarity and force anisotropy that drives CCM.

Cell Polarity and Migration: Emerging Role for the Endosomal Sorting Machinery

Physiology ◽  
2011 ◽  
Vol 26 (3) ◽  
pp. 171-180 ◽  
Author(s):  
Viola Hélène Lobert ◽  
Harald Stenmark
Keyword(s):  
Cell Migration ◽  
Cell Division ◽  
Cell Polarity ◽  
Tumor Suppressors ◽  
Potential Role ◽  
Endosomal Sorting ◽  
Escrt Machinery ◽  
Viral Budding ◽  
And Migration

The endosomal sorting complex required for transport (ESCRT) machinery has been implicated in the regulation of endosomal sorting, cell division, viral budding, autophagy, and cell signaling. Here, we review recent evidence that implicates ESCRTs in cell polarity and cell migration, and discuss the potential role of ESCRTs as tumor suppressors.

scholarly journals Mechanochemical feedback underlies coexistence of qualitatively distinct cell polarity patterns within diverse cell populations

2017 ◽  
Vol 114 (28) ◽  
pp. E5750-E5759 ◽  
Author(s):  
JinSeok Park ◽  
William R. Holmes ◽  
Sung Hoon Lee ◽  
Hong-Nam Kim ◽  
Deok-Ho Kim ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cell Polarity ◽  
Cell Types ◽  
Small Gtpases ◽  
Cell Polarization ◽  
Environmental Perturbations ◽  
Oscillatory Dynamic ◽  
Distinct Cell ◽  
Spatially Distributed ◽  
Directional Cell Migration

Cell polarization and directional cell migration can display random, persistent, and oscillatory dynamic patterns. However, it is not clear whether these polarity patterns can be explained by the same underlying regulatory mechanism. Here, we show that random, persistent, and oscillatory migration accompanied by polarization can simultaneously occur in populations of melanoma cells derived from tumors with different degrees of aggressiveness. We demonstrate that all of these patterns and the probabilities of their occurrence are quantitatively accounted for by a simple mechanism involving a spatially distributed, mechanochemical feedback coupling the dynamically changing extracellular matrix (ECM)–cell contacts to the activation of signaling downstream of the Rho-family small GTPases. This mechanism is supported by a predictive mathematical model and extensive experimental validation, and can explain previously reported results for diverse cell types. In melanoma, this mechanism also accounts for the effects of genetic and environmental perturbations, including mutations linked to invasive cell spread. The resulting mechanistic understanding of cell polarity quantitatively captures the relationship between population variability and phenotypic plasticity, with the potential to account for a wide variety of cell migration states in diverse pathological and physiological conditions.

scholarly journals Dynamic behavior of GFP–CLIP-170 reveals fast protein turnover on microtubule plus ends

2008 ◽  
Vol 180 (4) ◽  
pp. 729-737 ◽  
Author(s):  
Katharina A. Dragestein ◽  
Wiggert A. van Cappellen ◽  
Jeffrey van Haren ◽  
George D. Tsibidis ◽  
Anna Akhmanova ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cell Division ◽  
Cell Polarity ◽  
Protein Turnover ◽  
Structural Changes ◽  
Cellular Processes ◽  
High Affinity ◽  
Division Cell ◽  
Turn Over ◽  
Rate Limiting

Microtubule (MT) plus end–tracking proteins (+TIPs) specifically recognize the ends of growing MTs. +TIPs are involved in diverse cellular processes such as cell division, cell migration, and cell polarity. Although +TIP tracking is important for these processes, the mechanisms underlying plus end specificity of mammalian +TIPs are not completely understood. Cytoplasmic linker protein 170 (CLIP-170), the prototype +TIP, was proposed to bind to MT ends with high affinity, possibly by copolymerization with tubulin, and to dissociate seconds later. However, using fluorescence-based approaches, we show that two +TIPs, CLIP-170 and end-binding protein 3 (EB3), turn over rapidly on MT ends. Diffusion of CLIP-170 and EB3 appears to be rate limiting for their binding to MT plus ends. We also report that the ends of growing MTs contain a surplus of sites to which CLIP-170 binds with relatively low affinity. We propose that the observed loss of fluorescent +TIPs at plus ends does not reflect the behavior of single molecules but is a result of overall structural changes of the MT end.

Cell polarity and asymmetric cell division: the C. elegans early embryo

2012 ◽  
Vol 53 ◽  
pp. 1-14 ◽  
Author(s):  
Anna Noatynska ◽  
Monica Gotta
Keyword(s):  
Cell Migration ◽  
Cell Division ◽  
Cell Polarity ◽  
Asymmetric Cell Division ◽  
Early Embryo ◽  
Animal Cells ◽  
Par Proteins ◽  
C Elegans ◽  
Lethal Mutations ◽  
Tissue Organization

Cell polarity is crucial for many functions including cell migration, tissue organization and asymmetric cell division. In animal cells, cell polarity is controlled by the highly conserved PAR (PARtitioning defective) proteins. par genes have been identified in Caenorhabditis elegans in screens for maternal lethal mutations that disrupt cytoplasmic partitioning and asymmetric division. Although PAR proteins were identified more than 20 years ago, our understanding on how they regulate polarity and how they are regulated is still incomplete. In this chapter we review our knowledge of the processes of cell polarity establishment and maintenance, and asymmetric cell division in the early C. elegans embryo. We discuss recent findings that highlight new players in cell polarity and/or reveal the molecular details on how PAR proteins regulate polarity processes.

scholarly journals Integrin-mediated Adhesion Regulates Cell Polarity and Membrane Protrusion through the Rho Family of GTPases

2001 ◽  
Vol 12 (2) ◽  
pp. 265-277 ◽  
Author(s):  
Elisabeth A. Cox ◽  
Sarita K. Sastry ◽  
Anna Huttenlocher
Keyword(s):  
Cell Migration ◽  
Cell Polarity ◽  
Cross Talk ◽  
Cell Polarization ◽  
Stop Signal ◽  
Membrane Protrusion ◽  
Rhoa Activity ◽  
Rac1 Activity ◽  
Rho Family ◽  
Α5β1 Integrin

Integrin-mediated adhesion is a critical regulator of cell migration. Here we demonstrate that integrin-mediated adhesion to high fibronectin concentrations induces a stop signal for cell migration by inhibiting cell polarization and protrusion. On fibronectin, the stop signal is generated through α5β1 integrin-mediated signaling to the Rho family of GTPases. Specifically, Cdc42 and Rac1 activation exhibits a biphasic dependence on fibronectin concentration that parallels optimum cell polarization and protrusion. In contrast, RhoA activity increases with increasing substratum concentration. We find that cross talk between Cdc42 and Rac1 is required for substratum-stimulated protrusion, whereas RhoA activity is inhibitory. We also show that Cdc42 activity is inhibited by Rac1 activation, suggesting that Rac1 activity may down-regulate Cdc42 activity and promote the formation of stabilized rather than transient protrusion. Furthermore, expression of RhoA down-regulates Cdc42 and Rac1 activity, providing a mechanism whereby RhoA may inhibit cell polarization and protrusion. These findings implicate adhesion-dependent signaling as a mechanism to stop cell migration by regulating cell polarity and protrusion via the Rho family of GTPases.

EGL-27 is similar to a metastasis-associated factor and controls cell polarity and cell migration in C. elegans

Development ◽  
1999 ◽  
Vol 126 (5) ◽  
pp. 1055-1064 ◽  
Author(s):  
M.A. Herman ◽  
Q. Ch'ng ◽  
S.M. Hettenbach ◽  
T.M. Ratliff ◽  
C. Kenyon ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cell Division ◽  
T Cell ◽  
Cell Polarity ◽  
Wnt Pathway ◽  
Hox Gene ◽  
C Elegans ◽  
Metastatic Cells ◽  
Mosaic Analysis ◽  
Wnt Pathways

Mutations in the C. elegans gene egl-27 cause defects in cell polarity and cell migration: the polarity of the asymmetric T cell division is disrupted and the descendants of the migratory QL neuroblast migrate incorrectly because they fail to express the Hox gene mab-5. Both of these processes are known to be controlled by Wnt pathways. Mosaic analysis indicates that egl-27 function is required in the T cell for proper cell polarity. We cloned egl-27 and discovered that a domain of the predicted EGL-27 protein has similarity to Mta1, a mammalian factor overexpressed in metastatic cells. Overlaps in the phenotypes of egl-27 and Wnt pathway mutants suggest that the EGL-27 protein interacts with Wnt signaling pathways in C. elegans.

scholarly journals Coordination of tissue cell polarity by auxin transport and signaling

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Carla Verna ◽  
Sree Janani Ravichandran ◽  
Megan G Sawchuk ◽  
Nguyen Manh Linh ◽  
Enrico Scarpella
Keyword(s):  
Cell Polarity ◽  
Membrane Trafficking ◽  
Auxin Transport ◽  
Cell Polarization ◽  
Tissue Cell ◽  
Auxin Signaling ◽  
Vein Formation ◽  
Dependent Signal ◽  
Vein Patterning ◽  
Auxin Transporter

Plants coordinate the polarity of hundreds of cells during vein formation, but how they do so is unclear. The prevailing hypothesis proposes that GNOM, a regulator of membrane trafficking, positions PIN-FORMED auxin transporters to the correct side of the plasma membrane; the resulting cell-to-cell, polar transport of auxin would coordinate tissue cell polarity and induce vein formation. Contrary to predictions of the hypothesis, we find that vein formation occurs in the absence of PIN-FORMED or any other intercellular auxin-transporter; that the residual auxin-transport-independent vein-patterning activity relies on auxin signaling; and that a GNOM-dependent signal acts upstream of both auxin transport and signaling to coordinate tissue cell polarity and induce vein formation. Our results reveal synergism between auxin transport and signaling, and their unsuspected control by GNOM in the coordination of tissue cell polarity during vein patterning, one of the most informative expressions of tissue cell polarization in plants.

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