Role of non-canonical Wnt/Planar Cell Polarity signaling in gut-endoderm morphogenesis

2021 ◽  
Author(s):  
Anurag Kakkerla Balaraju
Keyword(s):  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Canonical Wnt ◽  
Gut Endoderm

The role of the non-canonical Wnt–planar cell polarity pathway in neural crest migration

2013 ◽  
Vol 457 (1) ◽  
pp. 19-26 ◽  
Author(s):  
Roberto Mayor ◽  
Eric Theveneau
Keyword(s):  
Neural Crest ◽  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Neural Crest Cells ◽  
Contact Inhibition ◽  
Stem Cell Population ◽  
Planar Cell Polarity Pathway ◽  
Canonical Wnt ◽  
Neural Crest Migration

The neural crest is an embryonic stem cell population whose migratory behaviour has been likened to malignant invasion. The neural crest, as does cancer, undergoes an epithelial-to-mesenchymal transition and migrates to colonize almost all the tissues of the embryo. Neural crest cells exhibit collective cell migration, moving in streams of high directionality. The migratory neural crest streams are kept in shape by the presence of negative signals in their vicinity. The directionality of the migrating neural crest is achieved by contact-dependent cell polarization, in a phenomenon called contact inhibition of locomotion. Two cells experiencing contact inhibition of locomotion move away from each other after collision. However, if the cell density is high only cells exposed to a free edge can migrate away from the cluster leading to the directional migration of the whole group. Recent work performed in chicks, zebrafish and frogs has shown that the non-canonical Wnt–PCP (planar cell polarity) pathway plays a major role in neural crest migration. PCP signalling controls contact inhibition of locomotion between neural crest cells by localizing different PCP proteins at the site of cell contact during collision and locally regulating the activity of Rho GTPases. Upon collision RhoA (ras homologue family member A) is activated, whereas Rac1 is inhibited at the contact between two migrating neural crest cells, leading to the collapse of protrusions and the migration of cells away from one another. The present review summarizes the mechanisms that control neural crest migration and focuses on the role of non-canonical Wnt or PCP signalling in this process.

scholarly journals Update on the Role of the Non-Canonical Wnt/Planar Cell Polarity Pathway in Neural Tube Defects

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1198 ◽  
Author(s):  
Wang ◽  
Marco ◽  
Capra ◽  
Kibar
Keyword(s):  
Cell Polarity ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
Planar Cell Polarity ◽  
Neural Tube Closure ◽  
Convergent Extension ◽  
Complex Genetics ◽  
Pcp Signaling ◽  
Canonical Wnt

Neural tube defects (NTDs), including spina bifida and anencephaly, represent the most severe and common malformations of the central nervous system affecting 0.7–3 per 1000 live births. They result from the failure of neural tube closure during the first few weeks of pregnancy. They have a complex etiology that implicate a large number of genetic and environmental factors that remain largely undetermined. Extensive studies in vertebrate models have strongly implicated the non-canonical Wnt/planar cell polarity (PCP) signaling pathway in the pathogenesis of NTDs. The defects in this pathway lead to a defective convergent extension that is a major morphogenetic process essential for neural tube elongation and subsequent closure. A large number of genetic studies in human NTDs have demonstrated an important role of PCP signaling in their etiology. However, the relative contribution of this pathway to this complex etiology awaits a better picture of the complete genetic architecture of these defects. The emergence of new genome technologies and bioinformatics pipelines, complemented with the powerful tool of animal models for variant interpretation as well as significant collaborative efforts, will help to dissect the complex genetics of NTDs. The ultimate goal is to develop better preventive and counseling strategies for families affected by these devastating conditions.

scholarly journals Glypican 4 regulates planar cell polarity of endoderm cells by controlling the localization of Cadherin 2

Development ◽  
2021 ◽  
Author(s):  
Anurag Kakkerla Balaraju ◽  
Bo Hu ◽  
Juan J Rodriguez ◽  
Matthew Murry ◽  
Fang Lin
Keyword(s):  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Molecular Mechanisms ◽  
Sulfate Proteoglycan ◽  
Endodermal Cell ◽  
Convergence And Extension ◽  
Pcp Signaling ◽  
Endodermal Cells ◽  
Canonical Wnt

Non-canonical Wnt/Planar Cell Polarity (Wnt/PCP) signaling has been implicated in endoderm morphogenesis. However, the underlying cellular and molecular mechanisms of this process are unclear. We found that during convergence and extension (C&E) in zebrafish, gut endodermal cells are polarized mediolaterally, with GFP-Vangl2 enriched at the anterior edges. Endoderm cell polarity is lost, and intercalation is impaired, in the absence of glypican 4 (gpc4), a heparan-sulfate proteoglycan that promotes Wnt/PCP signaling, suggesting that this signaling is required for endodermal cell polarity. Live imaging revealed that endoderm C&E is accomplished by polarized cell protrusions and junction remodeling, which are impaired in gpc4-deficient endodermal cells. Furthermore, in the absence of gpc4, Cadherin 2 expression on the endodermal cell surface is increased due to impaired Rab5c-mediated endocytosis, which partially accounts for the endodermal defects in these mutants.These findings indicate that Gpc4 regulates endodermal planar cell polarity during endoderm C&E by influencing localization of Cadherin 2. Thus, our study uncovers a new mechanism by which Gpc4 regulates planar cell polarity and reveals the role of Wnt/PCP signaling in endoderm morphogenesis.

scholarly journals Non-Canonical Wnt Signaling Regulates Cochlear Outgrowth and Planar Cell Polarity via Gsk3β Inhibition

2021 ◽  
Vol 9 ◽  
Author(s):  
Andre Landin Malt ◽  
Shaylyn Clancy ◽  
Diane Hwang ◽  
Alice Liu ◽  
Connor Smith ◽  
...  
Keyword(s):  
Wnt Signaling ◽  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Small Gtpase ◽  
Hair Bundle ◽  
Apical Surface ◽  
Canonical Wnt Signaling ◽  
Genetic Rescue ◽  
Genetic Ablation ◽  
Canonical Wnt

During development, sensory hair cells (HCs) in the cochlea assemble a stereociliary hair bundle on their apical surface with planar polarized structure and orientation. We have recently identified a non-canonical, Wnt/G-protein/PI3K signaling pathway that promotes cochlear outgrowth and coordinates planar polarization of the HC apical cytoskeleton and alignment of HC orientation across the cochlear epithelium. Here, we determined the involvement of the kinase Gsk3β and the small GTPase Rac1 in non-canonical Wnt signaling and its regulation of the planar cell polarity (PCP) pathway in the cochlea. We provided the first in vivo evidence for Wnt regulation of Gsk3β activity via inhibitory Ser9 phosphorylation. Furthermore, we carried out genetic rescue experiments of cochlear defects caused by blocking Wnt secretion. We showed that cochlear outgrowth was partially rescued by genetic ablation of Gsk3β but not by expression of stabilized β-catenin; while PCP defects, including hair bundle polarity and junctional localization of the core PCP proteins Fzd6 and Dvl2, were partially rescued by either Gsk3β ablation or constitutive activation of Rac1. Our results identify Gsk3β and likely Rac1 as downstream components of non-canonical Wnt signaling and mediators of cochlear outgrowth, HC planar polarity, and localization of a subset of core PCP proteins in the cochlea.

Role of the planar cell polarity pathway in regulating ectopic hair cell-like cells induced by Math1 and testosterone treatment

2015 ◽  
Vol 1615 ◽  
pp. 22-30 ◽  
Author(s):  
Xiao-yu Yang ◽  
Kai Jin ◽  
Rui Ma ◽  
Juan-mei Yang ◽  
Wen-wei Luo ◽  
...  
Keyword(s):  
Hair Cell ◽  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Testosterone Treatment ◽  
Planar Cell Polarity Pathway

scholarly journals Planar cell polarity in the larval epidermis of Drosophila and the role of microtubules

Open Biology ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 200290
Author(s):  
Stefano Pietra ◽  
KangBo Ng ◽  
Peter A. Lawrence ◽  
José Casal
Keyword(s):  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Published Data ◽  
Anterior Compartment ◽  
Intercellular Bridges ◽  
Gradient Model

We investigate planar cell polarity (PCP) in the Drosophila larval epidermis. The intricate pattern of denticles depends on only one system of PCP, the Dachsous/Fat system. Dachsous molecules in one cell bind to Fat molecules in a neighbour cell to make intercellular bridges. The disposition and orientation of these Dachsous–Fat bridges allows each cell to compare two neighbours and point its denticles towards the neighbour with the most Dachsous. Measurements of the amount of Dachsous reveal a peak at the back of the anterior compartment of each segment. Localization of Dachs and orientation of ectopic denticles help reveal the polarity of every cell. We discuss whether these findings support our gradient model of Dachsous activity. Several groups have proposed that Dachsous and Fat fix the direction of PCP via oriented microtubules that transport PCP proteins to one side of the cell. We test this proposition in the larval cells and find that most microtubules grow perpendicularly to the axis of PCP. We find no meaningful bias in the polarity of microtubules aligned close to that axis. We also reexamine published data from the pupal abdomen and find no evidence supporting the hypothesis that microtubular orientation draws the arrow of PCP.

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