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Journal articles on the topic 'Planar cell polarity pathway'

Author: Grafiati

Published: 25 May 2024

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1

Harrison, Carl, Hongyu Shao, Helen Strutt, and David Strutt. "Molecular mechanisms mediating asymmetric subcellular localisation of the core planar polarity pathway proteins." Biochemical Society Transactions 48, no. 4 (August 21, 2020): 1297–308. http://dx.doi.org/10.1042/bst20190404.

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Planar polarity refers to cellular polarity in an orthogonal plane to apicobasal polarity, and is seen across scales from molecular distributions of proteins to tissue patterning. In many contexts it is regulated by the evolutionarily conserved ‘core' planar polarity pathway that is essential for normal organismal development. Core planar polarity pathway components form asymmetric intercellular complexes that communicate polarity between neighbouring cells and direct polarised cell behaviours and the formation of polarised structures. The core planar polarity pathway consists of six structurally different proteins. In the fruitfly Drosophila melanogaster, where the pathway is best characterised, an intercellular homodimer of the seven-pass transmembrane protein Flamingo interacts on one side of the cell junction with the seven-pass transmembrane protein Frizzled, and on the other side with the four-pass transmembrane protein Strabismus. The cytoplasmic proteins Diego and Dishevelled are co-localised with Frizzled, and Prickle co-localises with Strabismus. Between these six components there are myriad possible molecular interactions, which could stabilise or destabilise the intercellular complexes and lead to their sorting into polarised distributions within cells. Post-translational modifications are key regulators of molecular interactions between proteins. Several post-translational modifications of core proteins have been reported to be of functional significance, in particular phosphorylation and ubiquitination. In this review, we discuss the molecular control of planar polarity and the molecular ecology of the core planar polarity intercellular complexes. Furthermore, we highlight the importance of understanding the spatial control of post-translational modifications in the establishment of planar polarity.

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2

Kacker, Sandeep, Varuneshwar Parsad, Naveen Singh, Daria Hordiichuk, Stacy Alvarez, Mahnoor Gohar, Anshu Kacker, and Sunil Kumar Rai. "Planar Cell Polarity Signaling: Coordinated Crosstalk for Cell Orientation." Journal of Developmental Biology 12, no. 2 (April 29, 2024): 12. http://dx.doi.org/10.3390/jdb12020012.

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The planar cell polarity (PCP) system is essential for positioning cells in 3D networks to establish the proper morphogenesis, structure, and function of organs during embryonic development. The PCP system uses inter- and intracellular feedback interactions between components of the core PCP, characterized by coordinated planar polarization and asymmetric distribution of cell populations inside the cells. PCP signaling connects the anterior–posterior to left–right embryonic plane polarity through the polarization of cilia in the Kupffer’s vesicle/node in vertebrates. Experimental investigations on various genetic ablation-based models demonstrated the functions of PCP in planar polarization and associated genetic disorders. This review paper aims to provide a comprehensive overview of PCP signaling history, core components of the PCP signaling pathway, molecular mechanisms underlying PCP signaling, interactions with other signaling pathways, and the role of PCP in organ and embryonic development. Moreover, we will delve into the negative feedback regulation of PCP to maintain polarity, human genetic disorders associated with PCP defects, as well as challenges associated with PCP.

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3

Wansleeben, Carolien, and Frits Meijlink. "The planar cell polarity pathway in vertebrate development." Developmental Dynamics 240, no. 3 (February 8, 2011): 616–26. http://dx.doi.org/10.1002/dvdy.22564.

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4

Wu, Gang, Jiao Ge, Xupei Huang, Yimin Hua, and Dezhi Mu. "Planar Cell Polarity Signaling Pathway in Congenital Heart Diseases." Journal of Biomedicine and Biotechnology 2011 (2011): 1–8. http://dx.doi.org/10.1155/2011/589414.

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Congenital heart disease (CHD) is a common cardiac disorder in humans. Despite many advances in the understanding of CHD and the identification of many associated genes, the fundamental etiology for the majority of cases remains unclear. The planar cell polarity (PCP) signaling pathway, responsible for tissue polarity inDrosophilaand gastrulation movements and cardiogenesis in vertebrates, has been shown to play multiple roles during cardiac differentiation and development. The disrupted function of PCP signaling is connected to some CHDs. Here, we summarize our current understanding of how PCP factors affect the pathogenesis of CHD.

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5

Werner, Michael E., Peter Hwang, Fawn Huisman, Peter Taborek, Clare C. Yu, and Brian J. Mitchell. "Actin and microtubules drive differential aspects of planar cell polarity in multiciliated cells." Journal of Cell Biology 195, no. 1 (September 26, 2011): 19–26. http://dx.doi.org/10.1083/jcb.201106110.

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Planar cell polarization represents the ability of cells to orient within the plane of a tissue orthogonal to the apical basal axis. The proper polarized function of multiciliated cells requires the coordination of cilia spacing and cilia polarity as well as the timing of cilia beating during metachronal synchrony. The planar cell polarity pathway and hydrodynamic forces have been shown to instruct cilia polarity. In this paper, we show how intracellular effectors interpret polarity to organize cellular morphology in accordance with asymmetric cellular function. We observe that both cellular actin and microtubule networks undergo drastic reorganization, providing differential roles during the polarized organization of cilia. Using computational angular correlation analysis of cilia orientation, we report a graded cellular organization downstream of cell polarity cues. Actin dynamics are required for proper cilia spacing, global coordination of cilia polarity, and coordination of metachronic cilia beating, whereas cytoplasmic microtubule dynamics are required for local coordination of polarity between neighboring cilia.

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6

Funato, Yosuke, Tatsuo Michiue, Takeshi Terabayashi, Akira Yukita, Hiroki Danno, Makoto Asashima, and Hiroaki Miki. "Nucleoredoxin regulates the Wnt/planar cell polarity pathway inXenopus." Genes to Cells 13, no. 9 (September 2008): 965–75. http://dx.doi.org/10.1111/j.1365-2443.2008.01220.x.

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7

LaMonica, Kristi A., Maya Bass, and Laura Grabel. "The planar cell polarity pathway regulates parietal endoderm outgrowth." Developmental Biology 306, no. 1 (June 2007): 371. http://dx.doi.org/10.1016/j.ydbio.2007.03.542.

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8

LaMonica, Kristi, Maya Bass, and Laura Grabel. "The planar cell polarity pathway directs parietal endoderm migration." Developmental Biology 330, no. 1 (June 2009): 44–53. http://dx.doi.org/10.1016/j.ydbio.2009.03.008.

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9

Peunova, Natalia, and Grigori Enikolopov. "P61. NO links planar cell polarity pathway with ciliogenesis." Nitric Oxide 19 (2008): 57. http://dx.doi.org/10.1016/j.niox.2008.06.158.

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10

Rocque, Brittany, and Elena Torban. "Planar Cell Polarity Pathway in Kidney Development and Function." Advances in Nephrology 2015 (February 25, 2015): 1–15. http://dx.doi.org/10.1155/2015/764682.

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The evolutionarily conserved planar cell polarity (PCP) signaling pathway controls tissue polarity within the plane orthogonal to the apical-basal axis. PCP was originally discovered in Drosophila melanogaster where it is required for the establishment of a uniform pattern of cell structures and appendages. In vertebrates, including mammals, the PCP pathway has been adapted to control various morphogenetic processes that are critical for tissue and organ development. These include convergent extension (crucial for neural tube closure and cochlear duct development) and oriented cell division (needed for tubular elongation), ciliary tilting that enables directional fluid flow, and other processes. Recently, strong evidence has emerged to implicate the PCP pathway in vertebrate kidney development. In this review, we will describe the experimental data revealing the role of PCP signaling in nephrogenesis and kidney disease.

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11

Axelrod, Jeffrey D., and Helen McNeill. "Coupling Planar Cell Polarity Signaling to Morphogenesis." Scientific World JOURNAL 2 (2002): 434–54. http://dx.doi.org/10.1100/tsw.2002.105.

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Epithelial cells and other groups of cells acquire a polarity orthogonal to their apical–basal axes, referred to as Planar Cell Polarity (PCP). The process by which these cells become polarized requires a signaling pathway using Frizzled as a receptor. Responding cells sense cues from their environment that provide directional information, and they translate this information into cellular asymmetry. Most of what is known about PCP derives from studies in the fruit fly,Drosophila. We review what is known about how cells translate an unknown signal into asymmetric cytoskeletal reorganization. We then discuss how the vertebrate processes of convergent extension and cochlear hair-cell development may relate toDrosophilaPCP signaling.

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12

Guillabert-Gourgues, Aude, Beatrice Jaspard-Vinassa, Marie-Lise Bats, Raj N. Sewduth, Nathalie Franzl, Claire Peghaire, Sylvie Jeanningros, et al. "Kif26b controls endothelial cell polarity through the Dishevelled/Daam1-dependent planar cell polarity–signaling pathway." Molecular Biology of the Cell 27, no. 6 (March 15, 2016): 941–53. http://dx.doi.org/10.1091/mbc.e14-08-1332.

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Angiogenesis involves the coordinated growth and migration of endothelial cells (ECs) toward a proangiogenic signal. The Wnt planar cell polarity (PCP) pathway, through the recruitment of Dishevelled (Dvl) and Dvl-associated activator of morphogenesis (Daam1), has been proposed to regulate cell actin cytoskeleton and microtubule (MT) reorganization for oriented cell migration. Here we report that Kif26b—a kinesin—and Daam1 cooperatively regulate initiation of EC sprouting and directional migration via MT reorganization. First, we find that Kif26b is recruited within the Dvl3/Daam1 complex. Using a three-dimensional in vitro angiogenesis assay, we show that Kif26b and Daam1 depletion impairs tip cell polarization and destabilizes extended vascular processes. Kif26b depletion specifically alters EC directional migration and mislocalized MT organizing center (MTOC)/Golgi and myosin IIB cell rear enrichment. Therefore the cell fails to establish a proper front–rear polarity. Of interest, Kif26b ectopic expression rescues the siDaam1 polarization defect phenotype. Finally, we show that Kif26b functions in MT stabilization, which is indispensable for asymmetrical cell structure reorganization. These data demonstrate that Kif26b, together with Dvl3/Daam1, initiates cell polarity through the control of PCP signaling pathway–dependent activation.

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13

Kim, Sun K., Siwei Zhang, Michael E. Werner, Eva J. Brotslaw, Jennifer W. Mitchell, Mohamed M. Altabbaa, and Brian J. Mitchell. "CLAMP/Spef1 regulates planar cell polarity signaling and asymmetric microtubule accumulation in the Xenopus ciliated epithelia." Journal of Cell Biology 217, no. 5 (March 7, 2018): 1633–41. http://dx.doi.org/10.1083/jcb.201706058.

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Most epithelial cells polarize along the axis of the tissue, a feature known as planar cell polarity (PCP). The initiation of PCP requires cell–cell signaling via the noncanonical Wnt/PCP pathway. Additionally, changes in the cytoskeleton both facilitate and reflect this polarity. We have identified CLAMP/Spef1 as a novel regulator of PCP signaling. In addition to decorating microtubules (MTs) and the ciliary rootlet, a pool of CLAMP localizes at the apical cell cortex. Depletion of CLAMP leads to the loss of PCP protein asymmetry, defects in cilia polarity, and defects in the angle of cell division. Additionally, depletion of CLAMP leads to a loss of the atypical cadherin-like molecule Celrs2, suggesting that CLAMP facilitates the stabilization of junctional interactions responsible for proper PCP protein localization. Depletion of CLAMP also affects the polarized organization of MTs. We hypothesize that CLAMP facilitates the establishment of cell polarity and promotes the asymmetric accumulation of MTs downstream of the establishment of proper PCP.

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14

Torban, Elena, and Sergei Y. Sokol. "Planar cell polarity pathway in kidney development, function and disease." Nature Reviews Nephrology 17, no. 6 (February 5, 2021): 369–85. http://dx.doi.org/10.1038/s41581-021-00395-6.

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15

Li, Xin, Heidi Hamm, Florence Marlow, and Lilianna Solnica-Krezel. "Gpr125 - a novel planar cell polarity pathway component in zebrafish." Developmental Biology 356, no. 1 (August 2011): 122. http://dx.doi.org/10.1016/j.ydbio.2011.05.071.

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16

Babayeva, Sima, Brittany Rocque, Lamine Aoudjit, Yulia Zilber, Jane Li, Cindy Baldwin, Hiroshi Kawachi, Tomoko Takano, and Elena Torban. "Planar Cell Polarity Pathway Regulates Nephrin Endocytosis in Developing Podocytes." Journal of Biological Chemistry 288, no. 33 (July 3, 2013): 24035–48. http://dx.doi.org/10.1074/jbc.m113.452904.

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17

Wen, Shu, Huiping Zhu, Wei Lu, Laura E. Mitchell, Gary M. Shaw, Edward J. Lammer, and Richard H. Finnell. "Planar cell polarity pathway genes and risk for spina bifida." American Journal of Medical Genetics Part A 152A, no. 2 (February 2010): 299–304. http://dx.doi.org/10.1002/ajmg.a.33230.

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18

Siletti, Kimberly, Basile Tarchini, and A. J. Hudspeth. "Daple coordinates organ-wide and cell-intrinsic polarity to pattern inner-ear hair bundles." Proceedings of the National Academy of Sciences 114, no. 52 (December 11, 2017): E11170—E11179. http://dx.doi.org/10.1073/pnas.1716522115.

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The establishment of planar polarization by mammalian cells necessitates the integration of diverse signaling pathways. In the inner ear, at least two systems regulate the planar polarity of sensory hair bundles. The core planar cell polarity (PCP) proteins coordinate the orientations of hair cells across the epithelial plane. The cell-intrinsic patterning of hair bundles is implemented independently by the G protein complex classically known for orienting the mitotic spindle. Although the primary cilium also participates in each of these pathways, its role and the integration of the two systems are poorly understood. We show that Dishevelled-associating protein with a high frequency of leucine residues (Daple) interacts with PCP and cell-intrinsic signals. Regulated by the cell-intrinsic pathway, Daple is required to maintain the polarized distribution of the core PCP protein Dishevelled and to position the primary cilium at the abneural edge of the apical surface. Our results suggest that the primary cilium or an associated structure influences the domain of cell-intrinsic signals that shape the hair bundle. Daple is therefore essential to orient and pattern sensory hair bundles.

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19

Segalen, Marion, and Yohanns Bellaïche. "Cell division orientation and planar cell polarity pathways." Seminars in Cell & Developmental Biology 20, no. 8 (October 2009): 972–77. http://dx.doi.org/10.1016/j.semcdb.2009.03.018.

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20

Artus, Cédric, Fabienne Glacial, Kayathiri Ganeshamoorthy, Nicole Ziegler, Maeva Godet, Thomas Guilbert, Stefan Liebner, and Pierre-Olivier Couraud. "The Wnt/Planar Cell Polarity Signaling Pathway Contributes to the Integrity of Tight Junctions in Brain Endothelial Cells." Journal of Cerebral Blood Flow & Metabolism 34, no. 3 (December 18, 2013): 433–40. http://dx.doi.org/10.1038/jcbfm.2013.213.

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Wnt morphogens released by neural precursor cells were recently reported to control blood–brain barrier (BBB) formation during development. Indeed, in mouse brain endothelial cells, activation of the Wnt/ β-catenin signaling pathway, also known as the canonical Wnt pathway, was shown to stabilize endothelial tight junctions (TJs) through transcriptional regulation of the expression of TJ proteins. Because Wnt proteins activate several distinct β-catenin-dependent and independent signaling pathways, this study was designed to assess whether the noncanonical Wnt/Par/aPKC planar cell polarity (PCP) pathway might also control TJ integrity in brain endothelial cells. First we established, in the hCMEC/D3 human brain endothelial cell line, that the Par/aPKC PCP complex colocalizes with TJs and controls apicobasal polarization. Second, using an siRNA approach, we showed that the Par/aPKC PCP complex regulates TJ stability and reassembling after osmotic shock. Finally, we provided evidence that Wnt5a signals in hCMEC/D3 cells through activation of the Par/aPKC PCP complex, independently of the Wnt canonical β-catenin-dependent pathway and significantly contributes to TJ integrity and endothelial apicobasal polarity. In conclusion, this study suggests that the Wnt/Par/aPKC PCP pathway, in addition to the Wnt/ β-catenin canonical pathway, is a key regulator of the BBB.

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21

Lawrence, Peter A., Gary Struhl, and José Casal. "Planar cell polarity: one or two pathways?" Nature Reviews Genetics 8, no. 7 (June 12, 2007): 555–63. http://dx.doi.org/10.1038/nrg2125.

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22

Walczyńska, Katarzyna S., Ling Zhu, and Yujun Liang. "Insights into the role of the Wnt signaling pathway in the regeneration of animal model systems." International Journal of Developmental Biology 67, no. 3 (2023): 65–78. http://dx.doi.org/10.1387/ijdb.220144yl.

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Regeneration enables the regrowth and restoration of missing body parts. It is a common phenomenon among animals. However, only some species exhibit remarkable regeneration capabilities and can regenerate organs such as limbs, lenses or hearts. Regeneration has been widely studied, thereby giving rise to new fields, such as regenerative medicine. Furthermore, regeneration has the potential to be applied to the human body. However, the molecular mechanisms governing this process should be elucidated first. Recent advancements in research methods have led to the identification of numerous signaling pathways involved in regeneration. One of them, the Wnt transduction pathway, is an ancient and evolutionarily conserved pathway that plays an important role in both embryonic development and regeneration. The Wnt pathway plays an important role during the regeneration process, as it is implicated in cell fate determination, cell migration, cell polarity and adult cell homeostasis. To date, two major Wnt pathways have been identified: the canonical (β-catenin dependent) pathway and the non-canonical pathway. The latter pathway can be further divided into planar cell polarity, the Wnt/Ca2+ pathway and the JNK pathway. In this review, we summarize the current state of knowledge regarding the Wnt signaling pathway and its role in regeneration, with a particular emphasis on key model species.

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23

Vladar, Eszter K., and Melanie Königshoff. "Noncanonical Wnt planar cell polarity signaling in lung development and disease." Biochemical Society Transactions 48, no. 1 (February 25, 2020): 231–43. http://dx.doi.org/10.1042/bst20190597.

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The planar cell polarity (PCP) signaling pathway is a potent developmental regulator of directional cell behaviors such as migration, asymmetric division and morphological polarization that are critical for shaping the body axis and the complex three-dimensional architecture of tissues and organs. PCP is considered a noncanonical Wnt pathway due to the involvement of Wnt ligands and Frizzled family receptors in the absence of the beta-catenin driven gene expression observed in the canonical Wnt cascade. At the heart of the PCP mechanism are protein complexes capable of generating molecular asymmetries within cells along a tissue-wide axis that are translated into polarized actin and microtubule cytoskeletal dynamics. PCP has emerged as an important regulator of developmental, homeostatic and disease processes in the respiratory system. It acts along other signaling pathways to create the elaborately branched structure of the lung by controlling the directional protrusive movements of cells during branching morphogenesis. PCP operates in the airway epithelium to establish and maintain the orientation of respiratory cilia along the airway axis for anatomically directed mucociliary clearance. It also regulates the establishment of the pulmonary vasculature. In adult tissues, PCP dysfunction has been linked to a variety of chronic lung diseases such as cystic fibrosis, chronic obstructive pulmonary disease, and idiopathic pulmonary arterial hypertension, stemming chiefly from the breakdown of proper tissue structure and function and aberrant cell migration during regenerative wound healing. A better understanding of these (impaired) PCP mechanisms is needed to fully harness the therapeutic opportunities of targeting PCP in chronic lung diseases.

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24

Gajos-Michniewicz, Anna, and Malgorzata Czyz. "WNT Signaling in Melanoma." International Journal of Molecular Sciences 21, no. 14 (July 9, 2020): 4852. http://dx.doi.org/10.3390/ijms21144852.

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WNT-signaling controls important cellular processes throughout embryonic development and adult life, so any deregulation of this signaling can result in a wide range of pathologies, including cancer. WNT-signaling is classified into two categories: β-catenin-dependent signaling (canonical pathway) and β-catenin-independent signaling (non-canonical pathway), the latter can be further divided into WNT/planar cell polarity (PCP) and calcium pathways. WNT ligands are considered as unique directional growth factors that contribute to both cell proliferation and polarity. Origin of cancer can be diverse and therefore tissue-specific differences can be found in WNT-signaling between cancers, including specific mutations contributing to cancer development. This review focuses on the role of the WNT-signaling pathway in melanoma. The current view on the role of WNT-signaling in cancer immunity as well as a short summary of WNT pathway-related drugs under investigation are also provided.

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25

Doyle, Kristy, Justin Hogan, Meagan Lester, and Simon Collier. "The Frizzled Planar Cell Polarity signaling pathway controls Drosophila wing topography." Developmental Biology 317, no. 1 (May 2008): 354–67. http://dx.doi.org/10.1016/j.ydbio.2008.02.041.

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26

LaMonica, Kristi, Maya Bass, and Laura Grabel. "Parietal endoderm migration is directed by the planar cell polarity pathway." Developmental Biology 319, no. 2 (July 2008): 542. http://dx.doi.org/10.1016/j.ydbio.2008.05.274.

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27

Bastock, R., and D. Strutt. "The planar polarity pathway promotes coordinated cell migration during Drosophila oogenesis." Development 134, no. 17 (August 1, 2007): 3055–64. http://dx.doi.org/10.1242/dev.010447.

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28

Cong, Feng, Liang Schweizer, and Harold Varmus. "Casein Kinase Iε Modulates the Signaling Specificities of Dishevelled." Molecular and Cellular Biology 24, no. 5 (March 1, 2004): 2000–2011. http://dx.doi.org/10.1128/mcb.24.5.2000-2011.2004.

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ABSTRACT Wnt signaling is critical to many aspects of development, and aberrant activation of the Wnt signaling pathway can cause cancer. Dishevelled (Dvl) protein plays a central role in this pathway by transducing the signal from the Wnt receptor complex to the β-catenin destruction complex. Dvl also plays a pivotal role in the planar cell polarity pathway that involves the c-Jun N-terminal kinase (JNK). How functions of Dvl are regulated in these two distinct pathways is not clear. We show that deleting the C-terminal two-thirds of Dvl, which includes the PDZ and DEP domains and is essential for Dvl-induced JNK activation, rendered the molecule a much more potent activator of the β-catenin pathway. We also found that casein kinase Iε (CKIε), a previously identified positive regulator of Wnt signaling, stimulated Dvl activity in the Wnt pathway, but dramatically inhibited Dvl activity in the JNK pathway. Consistent with this, overexpression of CKIε in Drosophila melanogaster stimulated Wnt signaling and disrupted planar cell polarity. We also observed a correlation between the localization and the signaling activity of Dvl in the β-catenin pathway and the JNK pathway. Furthermore, by using RNA interference, we demonstrate that the Drosophila CKIε homologue Double time positively regulates the β-catenin pathway through Dvl and negatively regulates the Dvl-induced JNK pathway. We suggest that CKIε functions as a molecular switch to direct Dvl from the JNK pathway to the β-catenin pathway, possibly by altering the conformation of the C terminus of Dvl.

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29

Classen, Anne-Kathrin, Kurt I. Anderson, Eric Marois, and Suzanne Eaton. "Hexagonal Packing of Drosophila Wing Epithelial Cells by the Planar Cell Polarity Pathway." Developmental Cell 9, no. 6 (December 2005): 805–17. http://dx.doi.org/10.1016/j.devcel.2005.10.016.

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30

Sheldahl, Laird C., Diane C. Slusarski, Petra Pandur, Jeffrey R. Miller, Michael Kühl, and Randall T. Moon. "Dishevelled activates Ca2+ flux, PKC, and CamKII in vertebrate embryos." Journal of Cell Biology 161, no. 4 (May 26, 2003): 769–77. http://dx.doi.org/10.1083/jcb.200211094.

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Wnt ligands and Frizzled (Fz) receptors have been shown to activate multiple intracellular signaling pathways. Activation of the Wnt–β-catenin pathway has been described in greatest detail, but it has been reported that Wnts and Fzs also activate vertebrate planar cell polarity (PCP) and Wnt–Ca2+ pathways. Although the intracellular protein Dishevelled (Dsh) plays a dual role in both the Wnt–β-catenin and the PCP pathways, its potential involvement in the Wnt–Ca2+ pathway has not been investigated. Here we show that a Dsh deletion construct, XDshΔDIX, which is sufficient for activation of the PCP pathway, is also sufficient for activation of three effectors of the Wnt–Ca2+ pathway: Ca2+ flux, PKC, and calcium/calmodulin-dependent protein kinase II (CamKII). Furthermore, we find that interfering with endogenous Dsh function reduces the activation of PKC by Xfz7 and interferes with normal heart development. These data suggest that the Wnt–Ca2+ pathway utilizes Dsh, thereby implicating Dsh as a component of all reported Fz signaling pathways.

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31

Babayeva, Sima, Yulia Zilber, and Elena Torban. "Planar cell polarity pathway regulates actin rearrangement, cell shape, motility, and nephrin distribution in podocytes." American Journal of Physiology-Renal Physiology 300, no. 2 (February 2011): F549—F560. http://dx.doi.org/10.1152/ajprenal.00566.2009.

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Glomerular podocytes are highly polarized cells characterized by dynamic actin-based foot processes (FPs). Neighboring FPs form specialized junctions, slit diaphragms (SDs), which prevent passage of proteins into the ultrafiltrate. The SD protein complex is linked to cytoskeletal actin filaments and mutations in SD proteins lead to a dramatic change in cell morphology; proteinuria is accompanied by FP retraction and loss of SD structure. Thus, organization of the podocyte cytoskeleton is tightly linked to filtration barrier function. In a variety of cell systems, cytoskeleton arrangement is regulated by the planar cell polarity (PCP) pathway. PCP signals lead to the appearance of highly organized cellular structures that support directional cell movement and oriented cell division. Derangement of the PCP pathway causes neural tube defects and cystic kidney disease in mice. Here, we establish that the PCP pathway regulates the cytoskeleton of podocytes. We identify expression of core PCP proteins in mouse kidney sections and of PCP transcripts in murine and human cultured podocytes. The pathway is functional since Wnt5a causes redistribution of PCP proteins Dishevelled and Daam1. We also show that Wnt5a treatment changes podocyte morphology, alters nephrin distribution, increases the number of stress fibers, and increases cell motility. In reciprocal experiments, siRNA depletion of the core PCP gene Vangl2 reduced the number of cell projections and decreased stress fibers and cell motility. Finally, we demonstrate direct interactions between Vangl2 and the SD protein, MAGI-2. This suggests that the PCP pathway may be directly linked to organization of the SD as well as to regulation of podocyte cytoskeleton. Our observations indicate that PCP signaling may play an important role both in podocyte development and FP cytoskeleton dynamics.

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32

Ayukawa, Tomonori, Masakazu Akiyama, Yasukazu Hozumi, Kenta Ishimoto, Junko Sasaki, Haruki Senoo, Takehiko Sasaki, and Masakazu Yamazaki. "Tissue flow regulates planar cell polarity independently of the Frizzled core pathway." Cell Reports 40, no. 12 (September 2022): 111388. http://dx.doi.org/10.1016/j.celrep.2022.111388.

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33

Dworkin, Sebastian, Stephen M. Jane, and Charbel Darido. "The planar cell polarity pathway in vertebrate epidermal development, homeostasis and repair." Organogenesis 7, no. 3 (July 2011): 202–8. http://dx.doi.org/10.4161/org.7.3.18431.

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34

Wada, Hironori, and Hitoshi Okamoto. "Roles of planar cell polarity pathway genes for neural migration and differentiation." Development, Growth & Differentiation 51, no. 3 (February 27, 2009): 233–40. http://dx.doi.org/10.1111/j.1440-169x.2009.01092.x.

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35

Kelly, Michael, and Ping Chen. "Shaping the mammalian auditory sensory organ by the planar cell polarity pathway." International Journal of Developmental Biology 51, no. 6-7 (2007): 535–47. http://dx.doi.org/10.1387/ijdb.072344mk.

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36

Kai, Masatake, Nina Buchan, Carl-Philipp Heisenberg, and Masazumi Tada. "06-P043 Regulation of planar cell polarity signalling by the prenylation pathway." Mechanisms of Development 126 (August 2009): S132. http://dx.doi.org/10.1016/j.mod.2009.06.269.

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37

Caddy, Jacinta, Tomasz Wilanowski, Charbel Darido, Sebastian Dworkin, Stephen B. Ting, Quan Zhao, Gerhard Rank, et al. "Epidermal Wound Repair Is Regulated by the Planar Cell Polarity Signaling Pathway." Developmental Cell 19, no. 1 (July 2010): 138–47. http://dx.doi.org/10.1016/j.devcel.2010.06.008.

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Caddy, Jacinta, Tomasz Wilanowski, Charbel Darido, Sebastian Dworkin, Stephen B. Ting, Quan Zhao, Gerhard Rank, et al. "Epidermal Wound Repair Is Regulated by the Planar Cell Polarity Signaling Pathway." Developmental Cell 19, no. 2 (August 2010): 353. http://dx.doi.org/10.1016/j.devcel.2010.08.003.

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Heinonen, Krista M., Juan Ruiz Vanegas, Deborah Lew, Jana Krosl, and Claude Perreault. "Wnt4 Enhances Murine Hematopoietic Progenitor Cell Expansion Through a Planar Cell Polarity-Like Pathway." PLoS ONE 6, no. 4 (April 26, 2011): e19279. http://dx.doi.org/10.1371/journal.pone.0019279.

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Bradley, Elizabeth W., and M. Hicham Drissi. "Wnt5b regulates mesenchymal cell aggregation and chondrocyte differentiation through the planar cell polarity pathway." Journal of Cellular Physiology 226, no. 6 (March 17, 2011): 1683–93. http://dx.doi.org/10.1002/jcp.22499.

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Wang, Irene-Yanran, Chen-Fang Chung, Sima Babayeva, Tamara Sogomonian, and Elena Torban. "Loss of Planar Cell Polarity Effector Fuzzy Causes Renal Hypoplasia by Disrupting Several Signaling Pathways." Journal of Developmental Biology 10, no. 1 (December 23, 2021): 1. http://dx.doi.org/10.3390/jdb10010001.

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In vertebrates, the planar cell polarity (PCP) pathway regulates tissue morphogenesis during organogenesis, including the kidney. Mutations in human PCP effector proteins have been associated with severe syndromic ciliopathies. Importantly, renal hypoplasia has been reported in some patients. However, the developmental disturbance that causes renal hypoplasia is unknown. Here, we describe the early onset of profound renal hypoplasia in mice homozygous for null mutation of the PCP effector gene, Fuzzy. We found that this phenotype is caused by defective branching morphogenesis of the ureteric bud (UB) in the absence of defects in nephron progenitor specification or in early steps of nephrogenesis. By using various experimental approaches, we show that the loss of Fuzzy affects multiple signaling pathways. Specifically, we found mild involvement of GDNF/c-Ret pathway that drives UB branching. We noted the deficient expression of molecules belonging to the Bmp, Fgf and Shh pathways. Analysis of the primary cilia in the UB structures revealed a significant decrease in ciliary length. We conclude that renal hypoplasia in the mouse Fuzzy mutants is caused by defective UB branching associated with dysregulation of ciliary and non-ciliary signaling pathways. Our work suggests a PCP effector-dependent pathogenetic mechanism that contributes to renal hypoplasia in mice and humans.

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Miyagi, Chiemi, Susumu Yamashita, Yusuke Ohba, Hisayoshi Yoshizaki, Michiyuki Matsuda, and Toshio Hirano. "STAT3 noncell-autonomously controls planar cell polarity during zebrafish convergence and extension." Journal of Cell Biology 166, no. 7 (September 27, 2004): 975–81. http://dx.doi.org/10.1083/jcb.200403110.

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Zebrafish signal transducer and activator of transcription 3 (STAT3) controls the cell movements during gastrulation. Here, we show that noncell-autonomous activity of STAT3 signaling in gastrula organizer cells controls the polarity of neighboring cells through Dishevelled-RhoA signaling in the Wnt-planar cell polarity (Wnt-PCP) pathway. In STAT3-depleted embryos, although all the known molecules in the Wnt-PCP pathway were expressed normally, the RhoA activity in lateral mesendodermal cells was down-regulated, resulting in severe cell polarization defects in convergence and extension movements identical to Strabismus-depleted embryos. Cell-autonomous activation of Wnt-PCP signaling by ΔN-dishevelled rescued the defect in cell elongation, but not the orientation of lateral mesendodermal cells in STAT3-depleted embryos. The defect in the orientation could be rescued by transplantation of shield cells having noncell-autonomous activity of STAT3 signaling. These results suggest that the cells undergoing convergence and extension movement may sense the gradient of signaling molecules, which are expressed in gastrula organizer by STAT3 and noncell-autonomously activate PCP signaling in neighboring cells during zebrafish gastrulation.

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Kim, Su Kyoung, Asako Shindo, Tae Joo Park, Edwin C. Oh, Srimoyee Ghosh, Ryan S. Gray, Richard A. Lewis, et al. "Planar Cell Polarity Acts Through Septins to Control Collective Cell Movement and Ciliogenesis." Science 329, no. 5997 (July 29, 2010): 1337–40. http://dx.doi.org/10.1126/science.1191184.

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The planar cell polarity (PCP) signaling pathway governs collective cell movements during vertebrate embryogenesis, and certain PCP proteins are also implicated in the assembly of cilia. The septins are cytoskeletal proteins controlling behaviors such as cell division and migration. Here, we identified control of septin localization by the PCP protein Fritz as a crucial control point for both collective cell movement and ciliogenesis in Xenopus embryos. We also linked mutations in human Fritz to Bardet-Biedl and Meckel-Gruber syndromes, a notable link given that other genes mutated in these syndromes also influence collective cell movement and ciliogenesis. These findings shed light on the mechanisms by which fundamental cellular machinery, such as the cytoskeleton, is regulated during embryonic development and human disease.

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Pickup, Amanda T., Michele L. Lamka, Qi Sun, Man Lun R. Yip, and Howard D. Lipshitz. "Control of photoreceptor cell morphology, planar polarity and epithelial integrity during Drosophila eye development." Development 129, no. 9 (May 1, 2002): 2247–58. http://dx.doi.org/10.1242/dev.129.9.2247.

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We report that the hindsight (hnt) gene, which encodes a nuclear zinc-finger protein, regulates cell morphology, cell fate specification, planar cell polarity and epithelial integrity during Drosophila retinal development. In the third instar larval eye imaginal disc, HNT protein expression begins in the morphogenetic furrow and is refined to cells in the developing photoreceptor cell clusters just before their determination as neurons. In hnt mutant larval eye tissue, furrow markers persist abnormally posterior to the furrow, there is a delay in specification of preclusters as cells exit the furrow, there are morphological defects in the preclusters and recruitment of cells into specific R cell fates often does not occur. Additionally, genetically mosaic ommatidia with one or more hnt mutant outer photoreceptor cells, have planar polarity defects that include achirality, reversed chirality and misrotation. Mutants in the JNK pathway act as dominant suppressors of the hnt planar polarity phenotype, suggesting that HNT functions to downregulate JUN kinase (JNK) signaling during the establishment of ommatidial planar polarity. HNT expression continues in the photoreceptor cells of the pupal retina. When an ommatidium contains four or more hnt mutant photoreceptor cells, both genetically mutant and genetically wild-type photoreceptor cells fall out of the retinal epithelium, indicating a role for HNT in maintenance of epithelial integrity. In the late pupal stages, HNT regulates the morphogenesis of rhabdomeres within individual photoreceptor cells and the separation of the rhabdomeres of adjacent photoreceptor cells. Apical F-actin is depleted in hnt mutant photoreceptor cells before the observed defects in cellular morphogenesis and epithelial integrity. The analyses presented here, together with our previous studies in the embryonic amnioserosa and tracheal system, show that HNT has a general role in regulation of the F-actin-based cytoskeleton, JNK signaling, cell morphology and epithelial integrity during development.

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Saling, Mark, Jordan K. Duckett, Ian Ackers, Karen Coschigano, Scott Jenkinson, and Ramiro Malgor. "Wnt5a / planar cell polarity signaling pathway in urothelial carcinoma, a potential prognostic biomarker." Oncotarget 8, no. 19 (March 3, 2017): 31655–65. http://dx.doi.org/10.18632/oncotarget.15877.

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Bosveld, F., I. Bonnet, B. Guirao, S. Tlili, Z. Wang, A. Petitalot, R. Marchand, et al. "Mechanical Control of Morphogenesis by Fat/Dachsous/Four-Jointed Planar Cell Polarity Pathway." Science 336, no. 6082 (April 12, 2012): 724–27. http://dx.doi.org/10.1126/science.1221071.

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VanderVorst, Kacey, Jason Hatakeyama, Anastasia Berg, Hyun Lee, and Kermit L. Carraway. "Cellular and molecular mechanisms underlying planar cell polarity pathway contributions to cancer malignancy." Seminars in Cell & Developmental Biology 81 (September 2018): 78–87. http://dx.doi.org/10.1016/j.semcdb.2017.09.026.

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Cai, Chunquan, and Ouyan Shi. "Genetic evidence in planar cell polarity signaling pathway in human neural tube defects." Frontiers of Medicine 8, no. 1 (December 4, 2013): 68–78. http://dx.doi.org/10.1007/s11684-014-0308-4.

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Hikasa, Hiroki, Mikihito Shibata, Ichiro Hiratani, and Masanori Taira. "TheXenopusreceptor tyrosine kinase Xror2 modulates morphogenetic movements of the axial mesoderm and neuroectoderm via Wnt signaling." Development 129, no. 22 (November 15, 2002): 5227–39. http://dx.doi.org/10.1242/dev.129.22.5227.

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The Spemann organizer plays a central role in neural induction, patterning of the neuroectoderm and mesoderm, and morphogenetic movements during early embryogenesis. By seeking genes whose expression is activated by the organizer-specific LIM homeobox gene Xlim-1 in Xenopusanimal caps, we isolated the receptor tyrosine kinase Xror2. Xror2 is expressed initially in the dorsal marginal zone, then in the notochord and the neuroectoderm posterior to the midbrain-hindbrain boundary. mRNA injection experiments revealed that overexpression of Xror2 inhibits convergent extension of the dorsal mesoderm and neuroectoderm in whole embryos, as well as the elongation of animal caps treated with activin, whereas it does not appear to affect cell differentiation of neural tissue and notochord. Interestingly, mutant constructs in which the kinase domain was point-mutated or deleted (named Xror2-TM) also inhibited convergent extension, and did not counteract the wild-type, suggesting that the ectodomain of Xror2 per se has activities that may be modulated by the intracellular domain. In relation to Wnt signaling for planar cell polarity, we observed: (1) the Frizzled-like domain in the ectodomain is required for the activity of wild-type Xror2 and Xror2-TM; (2) co-expression of Xror2 with Xwnt11, Xfz7, or both,synergistically inhibits convergent extension in embryos; (3) inhibition of elongation by Xror2 in activin-treated animal caps is reversed by co-expression of a dominant negative form of Cdc42 that has been suggested to mediate the planar cell polarity pathway of Wnt; and (4) the ectodomain of Xror2 interacts with Xwnts in co-immunoprecipitation experiments. These results suggest that Xror2 cooperates with Wnts to regulate convergent extension of the axial mesoderm and neuroectoderm by modulating the planar cell polarity pathway of Wnt.

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Bentzinger, C. Florian, Julia von Maltzahn, Nicolas A. Dumont, Danny A. Stark, Yu Xin Wang, Kevin Nhan, Jérôme Frenette, DDW Cornelison, and Michael A. Rudnicki. "Wnt7a stimulates myogenic stem cell motility and engraftment resulting in improved muscle strength." Journal of Cell Biology 205, no. 1 (April 7, 2014): 97–111. http://dx.doi.org/10.1083/jcb.201310035.

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Wnt7a/Fzd7 signaling stimulates skeletal muscle growth and repair by inducing the symmetric expansion of satellite stem cells through the planar cell polarity pathway and by activating the Akt/mTOR growth pathway in muscle fibers. Here we describe a third level of activity where Wnt7a/Fzd7 increases the polarity and directional migration of mouse satellite cells and human myogenic progenitors through activation of Dvl2 and the small GTPase Rac1. Importantly, these effects can be exploited to potentiate the outcome of myogenic cell transplantation into dystrophic muscles. We observed that a short Wnt7a treatment markedly stimulated tissue dispersal and engraftment, leading to significantly improved muscle function. Moreover, myofibers at distal sites that fused with Wnt7a-treated cells were hypertrophic, suggesting that the transplanted cells deliver activated Wnt7a/Fzd7 signaling complexes to recipient myofibers. Taken together, we describe a viable and effective ex vivo cell modulation process that profoundly enhances the efficacy of stem cell therapy for skeletal muscle.

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