scholarly journals Insect Wing Membrane Topography Is Determined by the Dorsal Wing Epithelium

2013 ◽  
Vol 3 (1) ◽  
pp. 5-8 ◽  
Author(s):  
Andrea D Belalcazar ◽  
Kristy Doyle ◽  
Justin Hogan ◽  
David Neff ◽  
Simon Collier
Keyword(s):  
Planar Cell Polarity ◽  
Parasitic Wasp ◽  
Ventral Surface ◽  
Wing Membrane ◽  
Genetic Studies ◽  
Insect Wing ◽  
Membrane Topography ◽  
Wing Hair ◽  
Pcp Signaling ◽  
Multiple Cells

Abstract The Drosophila wing consists of a transparent wing membrane supported by a network of wing veins. Previously, we have shown that the wing membrane cuticle is not flat but is organized into ridges that are the equivalent of one wing epithelial cell in width and multiple cells in length. These cuticle ridges have an anteroposterior orientation in the anterior wing and a proximodistal orientation in the posterior wing. The precise topography of the wing membrane is remarkable because it is a fusion of two independent cuticle contributions from the dorsal and ventral wing epithelia. Here, through morphological and genetic studies, we show that it is the dorsal wing epithelium that determines wing membrane topography. Specifically, we find that wing hair location and membrane topography are coordinated on the dorsal, but not ventral, surface of the wing. In addition, we find that altering Frizzled Planar Cell Polarity (i.e., Fz PCP) signaling in the dorsal wing epithelium alone changes the membrane topography of both dorsal and ventral wing surfaces. We also examined the wing morphology of two model Hymenopterans, the honeybee Apis mellifera and the parasitic wasp Nasonia vitripennis. In both cases, wing hair location and wing membrane topography are coordinated on the dorsal, but not ventral, wing surface, suggesting that the dorsal wing epithelium also controls wing topography in these species. Because phylogenomic studies have identified the Hymenotera as basal within the Endopterygota family tree, these findings suggest that this is a primitive insect character.

scholarly journals ATP6AP2 functions as a V-ATPase assembly factor in the endoplasmic reticulum

2018 ◽  
Vol 29 (18) ◽  
pp. 2156-2164 ◽  
Author(s):  
Maria Clara Guida ◽  
Tobias Hermle ◽  
Laurie A. Graham ◽  
Virginie Hauser ◽  
Margret Ryan ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Planar Cell Polarity ◽  
Transmembrane Protein ◽  
Type I ◽  
Genetic Studies ◽  
C Terminus ◽  
Assembly Factor ◽  
Pcp Signaling ◽  
Er Homeostasis

ATP6AP2 (also known as the [pro]renin receptor) is a type I transmembrane protein that can be cleaved into two fragments in the Golgi apparatus. While in Drosophila ATP6AP2 functions in the planar cell polarity (PCP) pathway, recent human genetic studies have suggested that ATP6AP2 could participate in the assembly of the V-ATPase in the endoplasmic reticulum (ER). Using a yeast model, we show here that the V-ATPase assembly factor Voa1 can functionally be replaced by Drosophila ATP6AP2. This rescue is even more efficient when coexpressing its binding partner ATP6AP1, indicating that these two proteins together fulfill Voa1 functions in higher organisms. Structure–function analyses in both yeast and Drosophila show that proteolytic cleavage is dispensable, while C-terminus-dependent ER retrieval is required for ATP6AP2 function. Accordingly, we demonstrate that both overexpression and lack of ATP6AP2 causes ER stress in Drosophila wing cells and that the induction of ER stress is sufficient to cause PCP phenotypes. In summary, our results suggest that full-length ATP6AP2 contributes to the assembly of the V-ATPase proton pore and that impairment of this function affects ER homeostasis and PCP signaling.

scholarly journals Planar Cell Polarity: The Frizzled Homophobic Signal

2019 ◽  
Author(s):  
José-Eduardo Gomes
Keyword(s):  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Spatial Information ◽  
Transmembrane Protein ◽  
Adjacent Cell ◽  
Signaling Mechanism ◽  
Insect Wing ◽  
Crucial Feature ◽  
Pcp Signaling ◽  
Core Genes

The cell’s capacity to integrate and respond to spatial information is a crucial feature of morphogenesis and development. The Planar Cell Polarity (PCP) pathway is a signaling mechanism, widely conserved across metazoans, providing spatial orientation along the plane of an epithelium in morphogenic processes ranging from insect wing patterning to mammalian cochleae. Although the core genes involved in the PCP pathway have been molecularly identified in the 1990s, the PCP signaling mechanism remains controversial. In this article I discuss the main players and previous models of PCP signaling reported in the literature, and propose a new model. According to it PCP is established through an homophobic signal by transmembrane protein Frizzled (Fz): 1) a Fz signal in one cell repeals Fz itself in the adjacent cell, thereby generating symmetry breaking; 2) the instructive PCP signal is conveyed through Fz interaction with atypical cadherin Flamingo (Fmi). More broadly, homophobic signaling may represent a novel mechanism for cell-cell signaling of spatial information through modulation of cell adhesion rather than canonical ligand-receptor binding.

Multivariate analysis of geographic variation in Darevskia clarkorum (Darevsky & Vedmederja, 1977), correlation with geographic and climatic parameters, and true status of Darevskia dryada (Darevsky & Tuniyev, 1997)

Zootaxa ◽  
2021 ◽  
Vol 4990 (1) ◽  
pp. 1-22
Author(s):  
OSCAR ARRIBAS ◽  
KAMİL CANDAN ◽  
YUSUF KUMLUTA ◽  
ÇETİN ILGAZ
Keyword(s):  
Ventral Surface ◽  
Activity Period ◽  
Correct Identification ◽  
Adult Males ◽  
Climatic Parameters ◽  
Genetic Studies ◽  
Temperature And Precipitation ◽  
Valid Taxon ◽  
Larger Sample

All the Turkish populations studied, both those previously assigned to D. dryada (Subaşı and Yoldere villages, near Hopa) and those attributed to D. clarkorum (the largest sample studied so far, 177 specimens in total), are indistinguishable from each other and therefore must all be ascribed to the natural variability of a monotypic D. clarkorum. The Georgian specimens from the Type Locality of D. dryada (Charnaly river gorge, Chevachauri district) are clearly different, so that taxon cannot be considered a simple synonym for D. clarkorum, but as a valid taxon, although its proper status (more probably as a subspecies of D. clarkorum), is yet to be clarified. It is a highly threatened population, so studies should be done in vivo or with as low intrusiveness as possible.                 Darevskia dryada is clearly larger (SVL) than any D. clarkorum studied, with strongly longer heads and pilei in adult males (and hence more teeth in dentary bone), and higher dorsalia counts. There also seem to be (but need to be studied in a larger sample) more longitudinal rows of temporal scales between tympanic and parietal plates, a tendency to have more supralabial scales; comparatively smaller values for longitudinal rows of scales on the ventral surface of the thigh between the femoral pores and the outer row of enlarged scales, and higher collaria, and circumanalia scales. Other differences in femoralia and gularia are also reflected in Darevsky & Tuniyev’s (1997) tables and should also be investigated with more Georgian specimens.                 Two supposed discriminant characters, the frontonasal index and the presence of developed masseteric, are not valid. The frontonasal index does not discriminate both taxa; D dryada specimens fall inside the variation of D. clarkorum for this character. Also the presence of a developed masseteric plate is supposed to be rare if at all in D. clarkorum but always present in D. dryada; however, it appears in nearly 75% of D. clarkorum studied and in all D. dyada, so is also no longer valid for taxa discrimination.                 Although very similar, D. clarkorum and D. dryada are morphologically different, and genetic studies (as the unpublished results mentioned by Fu, 1999) do not make the provenance of the specimens clear, and hence the correct identification of the supposed specimens of D. dryada used.                 There are no geographical clines in D. clarkorum. However, as stated by Schmidtler et al. (2002), there is an inverse relationship between altitude and dorsalia values in D. clarkorum. Both the general differentiation between populations and the scalation (dorsalia) appear statistically correlated with the altitude and also with latitude (being both factors not strictly the same). The correlation seems to be stronger with morphology in general (multiple scalation characters and head biometry) than only with dorsalia. In the case of the general differentiation among samples, it is also significantly correlated with temperatures during the activity period (April-September) and with precipitation during incubation (July-August). As these climatic parameters of temperature and precipitation are not directly correlated with the dorsalia variation, the relation with altitude (and perhaps latitude) must be linked to some other climatic parameter not studied here, perhaps solar radiation or evapotranspiration.  

scholarly journals Coupling Planar Cell Polarity Signaling to Morphogenesis

2002 ◽  
Vol 2 ◽  
pp. 434-454 ◽  
Author(s):  
Jeffrey D. Axelrod ◽  
Helen McNeill
Keyword(s):  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Fruit Fly ◽  
Convergent Extension ◽  
Cytoskeletal Reorganization ◽  
Directional Information ◽  
Cochlear Hair Cell ◽  
Cellular Asymmetry ◽  
Pcp Signaling ◽  
Unknown Signal

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.

scholarly journals SHROOM3 is a novel component of the planar cell polarity pathway whose disruption causes congenital heart disease

2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Alison Schmidt ◽  
Matthew Durbin, MS MD ◽  
James O’Kane, MS ◽  
Stephanie M. Ware, MD PHD
Keyword(s):  
Congenital Heart Disease ◽  
Heart Disease ◽  
Signaling Pathway ◽  
Cell Polarity ◽  
Congenital Heart ◽  
Planar Cell Polarity ◽  
Cardiac Development ◽  
Genetic Interaction ◽  
Compound Heterozygous ◽  
Pcp Signaling

Congenital heart disease (CHD) is the most common cause of death due to birth defects. Despite CHD frequency, the etiology remains mostly unknown. Understanding CHD genetics and elucidating disease mechanism will help establish prognosis, identify comorbidity risks, and develop targeted therapies. CHD often results from disrupted cytoarchitecture and signaling pathways. We have identified a novel CHD candidate SHROOM3, a protein associated with the actin cytoskeleton and the Wnt/Planar Cell Polarity (PCP) signaling pathway. SHROOM3 induces actomyosin constriction within the apical side of cells and is implicated in neural tube defects and chronic renal failure in humans. A recent study demonstrated that SHROOM3 interacts with Dishevelled2 (DVL2), a component of the PCP signaling pathway, suggesting that SHROOM3 serves as an important link between acto-myosin constriction and PCP signaling. PCP signaling establishes cell polarity required for multiple developmental processes, and is required for cardiac development. In Preliminary data we utilized a Shroom3 gene-trap mouse (Shroom3gt/gt) to demonstrated that SHROOM3 disruption leads to cardiac defects phenocopy PCP disruption. We also demonstrate that patients with CHD phenotypes have rare and potentially damaging SHROOM3 variants within SHROOM3’s PCP-binding domain. We hypothesize SHROOM3 is a novel terminal effector of PCP signaling, and disruption is a novel contributor to CHD. To test this, we assessed genetic interaction between SHROOM3 and PCP during cardiac development and the ultimate effect on cell structure and movement. Heterozygous Shroom3+/gt mice and heterozygous Dvl2 +/- mice are phenotypically normal. We demonstrated genetic interaction between SHROOM3 and PCP signaling by generating compound heterozygous Shroom3+/gt ;Dvl2 +/- mice and identifying a Double Outlet Right Ventricle and Ventricular Septal Defect in one embryo. We also observed fewer compound heterozygous mice than anticipated by Mendelian rations (observed: 18.4%; expected: 25%; n=76), suggesting potential lethality in utero. Immunohistochemistry demonstrates disrupted actomyosin in the SHROOM3gt/gt mice, characteristic of PCP disruption. These data help strengthen SHROOM3 as a novel CHD candidate gene and a component of the PCP Signaling pathway. Further characterization of this gene is important for CHD diagnosis and therapeutic development.

scholarly journals Particle Adhesion Measurements on Insect Wing Membranes Using Atomic Force Microscopy

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Gregory S. Watson ◽  
Bronwen W. Cribb ◽  
Jolanta A. Watson
Keyword(s):  
Atomic Force Microscopy ◽  
Surface Area ◽  
Wing Surface ◽  
Silica Spheres ◽  
Wing Membrane ◽  
Insect Wing ◽  
Force Microscopy ◽  
Plant Matter ◽  
Atomic Force ◽  
Eurema Hecabe

Many insects have evolved refined self-cleaning membrane structuring to contend with an environment that presents a range of potential contaminates. Contamination has the potential to reduce or interfere with the primary functioning of the wing membrane or affect other wing cuticle properties, (for example, antireflection). Insects will typically encounter a variety of air-borne contaminants which include plant matter and soil fragments. Insects with relatively long or large wings may be especially susceptible to fouling due to the high-wing surface area and reduced ability to clean their extremities. In this study we have investigated the adhesion of particles (pollens and hydrophilic silica spheres) to wing membranes of the super/hydrophobic cicada (Thopha sessiliba), butterfly (Eurema hecabe), and the hydrophilic wing of flower wasp (Scolia soror). The adhesional forces with both hydrophobic insects was significantly lower for all particle types than the hydrophilic insect species studied.

scholarly journals Planar Cell Polarity Signaling Pathway in Congenital Heart Diseases

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Gang Wu ◽  
Jiao Ge ◽  
Xupei Huang ◽  
Yimin Hua ◽  
Dezhi Mu
Keyword(s):  
Signaling Pathway ◽  
Cell Polarity ◽  
Congenital Heart ◽  
Planar Cell Polarity ◽  
Heart Diseases ◽  
Multiple Roles ◽  
Cardiac Differentiation ◽  
Tissue Polarity ◽  
Cardiac Disorder ◽  
Pcp Signaling

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.

scholarly journals The PCP effector Fuzzy controls cilial assembly and signaling by recruiting Rab8 and Dishevelled to the primary cilium

2013 ◽  
Vol 24 (5) ◽  
pp. 555-565 ◽  
Author(s):  
Yulia Zilber ◽  
Sima Babayeva ◽  
Jung Hwa Seo ◽  
Jia Jia Liu ◽  
Steven Mootin ◽  
...  
Keyword(s):  
Basal Body ◽  
Primary Cilium ◽  
Planar Cell Polarity ◽  
Primary Cilia ◽  
Wnt Pathway ◽  
Vertebrate Development ◽  
Cellular Processes ◽  
Ciliary Function ◽  
Pcp Signaling ◽  
Canonical Wnt

The planar cell polarity (PCP) pathway controls multiple cellular processes during vertebrate development. Recently the PCP pathway was implicated in ciliogenesis and in ciliary function. The primary cilium is an apically projecting solitary organelle that is generated via polarized intracellular trafficking. Because it acts as a signaling nexus, defects in ciliogenesis or cilial function cause multiple congenital anomalies in vertebrates. Loss of the PCP effector Fuzzy affects PCP signaling and formation of primary cilia; however, the mechanisms underlying these processes are largely unknown. Here we report that Fuzzy localizes to the basal body and ciliary axoneme and is essential for ciliogenesis by delivering Rab8 to the basal body and primary cilium. Fuzzy appears to control subcellular localization of the core PCP protein Dishevelled, recruiting it to Rab8-positive vesicles and to the basal body and cilium. We show that loss of Fuzzy results in inhibition of PCP signaling and hyperactivation of the canonical WNT pathway. We propose a mechanism by which Fuzzy participates in ciliogenesis and affects both canonical WNT and PCP signaling.

scholarly journals Planar Cell Polarity Acts Through Septins to Control Collective Cell Movement and Ciliogenesis

Science ◽  
2010 ◽  
Vol 329 (5997) ◽  
pp. 1337-1340 ◽  
Author(s):  
Su Kyoung Kim ◽  
Asako Shindo ◽  
Tae Joo Park ◽  
Edwin C. Oh ◽  
Srimoyee Ghosh ◽  
...  
Keyword(s):  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Control Point ◽  
Cell Movement ◽  
Cytoskeletal Proteins ◽  
Pcp Signaling ◽  
Cellular Machinery ◽  
And Migration ◽  
Controlling Behaviors ◽  
Shed Light

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.

scholarly journals BMP promotes motility and represses growth of smooth muscle cells by activation of tandem Wnt pathways

2011 ◽  
Vol 192 (1) ◽  
pp. 171-188 ◽  
Author(s):  
Vinicio A. de Jesus Perez ◽  
Ziad Ali ◽  
Tero-Pekka Alastalo ◽  
Fumiaki Ikeno ◽  
Hirofumi Sawada ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Planar Cell Polarity ◽  
Bone Morphogenetic Protein 2 ◽  
Dependent Manner ◽  
Morphogenetic Protein ◽  
Injury Model ◽  
Pcp Signaling ◽  
Integrin Linked Kinase ◽  
Wnt Pathways

We present a novel cell-signaling paradigm in which bone morphogenetic protein 2 (BMP-2) consecutively and interdependently activates the wingless (Wnt)–β-catenin (βC) and Wnt–planar cell polarity (PCP) signaling pathways to facilitate vascular smooth muscle motility while simultaneously suppressing growth. We show that BMP-2, in a phospho-Akt–dependent manner, induces βC transcriptional activity to produce fibronectin, which then activates integrin-linked kinase 1 (ILK-1) via α4-integrins. ILK-1 then induces the Wnt–PCP pathway by binding a proline-rich motif in disheveled (Dvl) and consequently activating RhoA-Rac1–mediated motility. Transfection of a Dvl mutant that binds βC without activating RhoA-Rac1 not only prevents BMP-2–mediated vascular smooth muscle cell motility but promotes proliferation in association with persistent βC activity. Interfering with the Dvl-dependent Wnt–PCP activation in a murine stented aortic graft injury model promotes extensive neointima formation, as shown by optical coherence tomography and histopathology. We speculate that, in response to injury, factors that subvert BMP-2–mediated tandem activation of Wnt–βC and Wnt–PCP pathways contribute to obliterative vascular disease in both the systemic and pulmonary circulations.

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