scholarly journals Prickle1mutation causes planar cell polarity and directional cell migration defects associated with cardiac outflow tract anomalies and other structural birth defects

Biology Open ◽  
2016 ◽  
Vol 5 (3) ◽  
pp. 323-335 ◽  
Author(s):  
Brian C. Gibbs ◽  
Rama Rao Damerla ◽  
Eszter K. Vladar ◽  
Bishwanath Chatterjee ◽  
Yong Wan ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cell Polarity ◽  
Birth Defects ◽  
Planar Cell Polarity ◽  
Outflow Tract ◽  
Directional Cell Migration ◽  
Cardiac Outflow

scholarly journals The core planar cell polarity gene, Vangl2 , directs adult corneal epithelial cell alignment and migration

2016 ◽  
Vol 3 (10) ◽  
pp. 160658 ◽  
Author(s):  
Amy S. Findlay ◽  
D. Alessio Panzica ◽  
Petr Walczysko ◽  
Amy B. Holt ◽  
Deborah J. Henderson ◽  
...  
Keyword(s):  
Cell Migration ◽  
Epithelial Cells ◽  
Cell Polarity ◽  
Corneal Epithelium ◽  
Planar Cell Polarity ◽  
Corneal Epithelial Cell ◽  
Corneal Epithelial Cells ◽  
Corneal Epithelial ◽  
The Core

This study shows that the core planar cell polarity (PCP) genes direct the aligned cell migration in the adult corneal epithelium, a stratified squamous epithelium on the outer surface of the vertebrate eye. Expression of multiple core PCP genes was demonstrated in the adult corneal epithelium. PCP components were manipulated genetically and pharmacologically in human and mouse corneal epithelial cells in vivo and in vitro . Knockdown of VANGL2 reduced the directional component of migration of human corneal epithelial (HCE) cells without affecting speed. It was shown that signalling through PCP mediators, dishevelled, dishevelled-associated activator of morphogenesis and Rho-associated protein kinase directs the alignment of HCE cells by affecting cytoskeletal reorganization. Cells in which VANGL2 was disrupted tended to misalign on grooved surfaces and migrate across, rather than parallel to the grooves. Adult corneal epithelial cells in which Vangl2 had been conditionally deleted showed a reduced rate of wound-healing migration. Conditional deletion of Vangl2 in the mouse corneal epithelium ablated the normal highly stereotyped patterns of centripetal cell migration in vivo from the periphery (limbus) to the centre of the cornea. Corneal opacity owing to chronic wounding is a major cause of degenerative blindness across the world, and this study shows that Vangl2 activity is required for directional corneal epithelial migration.

scholarly journals Connexin43 Modulates Cell Polarity and Directional Cell Migration by Regulating Microtubule Dynamics

PLoS ONE ◽  
2011 ◽  
Vol 6 (10) ◽  
pp. e26379 ◽  
Author(s):  
Richard Francis ◽  
Xin Xu ◽  
Hyunsoo Park ◽  
Chin-Jen Wei ◽  
Stephen Chang ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cell Polarity ◽  
Microtubule Dynamics ◽  
Directional Cell Migration

scholarly journals Wdpcp, a PCP Protein Required for Ciliogenesis, Regulates Directional Cell Migration and Cell Polarity by Direct Modulation of the Actin Cytoskeleton

PLoS Biology ◽  
2013 ◽  
Vol 11 (11) ◽  
pp. e1001720 ◽  
Author(s):  
Cheng Cui ◽  
Bishwanath Chatterjee ◽  
Thomas P. Lozito ◽  
Zhen Zhang ◽  
Richard J. Francis ◽  
...  
Keyword(s):  
Cell Migration ◽  
Actin Cytoskeleton ◽  
Cell Polarity ◽  
Direct Modulation ◽  
Directional Cell Migration

scholarly journals A small part of myosin IIB takes on a big role in cell polarity

2015 ◽  
Vol 209 (1) ◽  
pp. 11-12 ◽  
Author(s):  
Aidan M. Fenix ◽  
Dylan T. Burnette
Keyword(s):  
Cell Migration ◽  
Cell Polarity ◽  
Nonmuscle Myosin ◽  
New Paradigm ◽  
Cell Biol ◽  
Directional Cell Migration

A migrating cell must establish front-to-back polarity in order to move. In this issue, Juanes-Garcia et al. (2015. J. Cell Biol. http://dx.doi.org/10.1083/jcb.201407059) report that a short serine-rich motif in nonmuscle myosin IIB is required to establish the cell’s rear. This motif represents a new paradigm for what determines directional cell migration.

scholarly journals Homer3 regulates the establishment of neutrophil polarity

2015 ◽  
Vol 26 (9) ◽  
pp. 1629-1639 ◽  
Author(s):  
Julie Wu ◽  
Anne Pipathsouk ◽  
A. Keizer-Gunnink ◽  
F. Fusetti ◽  
W. Alkema ◽  
...  
Keyword(s):  
Cell Migration ◽  
Rna Interference ◽  
Cell Polarity ◽  
Actin Polymerization ◽  
Actin Assembly ◽  
Rac Gtpase ◽  
Gpcr Activation ◽  
Phosphoinositide 3 Kinase ◽  
Directional Cell Migration ◽  
Kinetics Of

Most chemoattractants rely on activation of the heterotrimeric G-protein Gαi to regulate directional cell migration, but few links from Gαi to chemotactic effectors are known. Through affinity chromatography using primary neutrophil lysate, we identify Homer3 as a novel Gαi2-binding protein. RNA interference–mediated knockdown of Homer3 in neutrophil-like HL-60 cells impairs chemotaxis and the establishment of polarity of phosphatidylinositol 3,4,5-triphosphate (PIP3) and the actin cytoskeleton, as well as the persistence of the WAVE2 complex. Most previously characterized proteins that are required for cell polarity are needed for actin assembly or activation of core chemotactic effectors such as the Rac GTPase. In contrast, Homer3-knockdown cells show normal magnitude and kinetics of chemoattractant-induced activation of phosphoinositide 3-kinase and Rac effectors. Chemoattractant-stimulated Homer3-knockdown cells also exhibit a normal initial magnitude of actin polymerization but fail to polarize actin assembly and intracellular PIP3 and are defective in the initiation of cell polarity and motility. Our data suggest that Homer3 acts as a scaffold that spatially organizes actin assembly to support neutrophil polarity and motility downstream of GPCR activation.

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 Muscularization of the Mesenchymal Outlet Septum during Cardiac Development

2020 ◽  
Vol 7 (4) ◽  
pp. 51
Author(s):  
Maurice J. B. van den Hoff ◽  
Andy Wessels
Keyword(s):  
Cell Polarity ◽  
Essential Role ◽  
Planar Cell Polarity ◽  
Cardiac Development ◽  
In Vitro Models ◽  
Outflow Tract ◽  
Heart Tube ◽  
Tgfβ Signaling ◽  
Experimental Approaches

After the formation of the linear heart tube, it becomes divided into right and left components by the process of septation. Relatively late during this process, within the developing outflow tract, the initially mesenchymal outlet septum becomes muscularized as the result of myocardialization. Myocardialization is defined as the process in which existing cardiomyocytes migrate into flanking mesenchyme. Studies using genetically modified mice, as well as experimental approaches using in vitro models, demonstrate that Wnt and TGFβ signaling play an essential role in the regulation of myocardialization. They also show the significance of the interaction between cardiomyocytes, endocardial derived cells, neural crest cells, and the extracellular matrix. Interestingly, Wnt-mediated non-canonical planar cell polarity signaling was found to be a crucial regulator of myocardialization in the outlet septum and Wnt-mediated canonical β-catenin signaling is an essential regulator of the expansion of mesenchymal cells populating the outflow tract cushions.

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