scholarly journals Jak-Stat pathway induces Drosophila follicle elongation by a gradient of apical contractility

2017 ◽  
Author(s):  
Hervé Alégot ◽  
Pierre Pouchin ◽  
Olivier Bardot ◽  
Vincent Mirouse
Keyword(s):  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Myosin Ii ◽  
Cell Polarization ◽  
Follicular Epithelium ◽  
Morphogen Gradient ◽  
Apical Constriction ◽  
Activity Inhibition ◽  
Apical Domain ◽  
Stat Pathway

AbstractTissue elongation and its control by spatiotemporal signals is a major developmental question. Currently, it is thought that Drosophila ovarian follicular epithelium elongation requires the planar polarization of the basal domain cytoskeleton and of the extra-cellular matrix, associated with a dynamic process of rotation around the anteroposterior axis. Here we show, by careful kinetic analysis of fat2 mutants, that neither basal planar polarization nor rotation is required during a first phase of follicle elongation. Conversely, a JAK-STAT signaling gradient from each follicle pole orients early elongation. JAK-STAT controls apical pulsatile contractions, and Myosin II activity inhibition affects both pulses and early elongation. Early elongation is associated with apical constriction at the poles and oriented cell rearrangements, but without any visible planar cell polarization of the apical domain. Thus, a morphogen gradient can trigger tissue elongation via a control of cell pulsing and without planar cell polarity requirement.Impact StatementFollicle elongation does not rely solely on the basal side of the cells but also requires a mechanism integrating a developmental cue with a morphogenetic process involving their apical domain.

scholarly journals Jak-Stat pathway induces Drosophila follicle elongation by a gradient of apical contractility

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Hervé Alégot ◽  
Pierre Pouchin ◽  
Olivier Bardot ◽  
Vincent Mirouse
Keyword(s):  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Myosin Ii ◽  
Cell Polarization ◽  
Follicular Epithelium ◽  
Morphogen Gradient ◽  
Apical Constriction ◽  
Activity Inhibition ◽  
Apical Domain ◽  
Stat Pathway

Tissue elongation and its control by spatiotemporal signals is a major developmental question. Currently, it is thought that Drosophila ovarian follicular epithelium elongation requires the planar polarization of the basal domain cytoskeleton and of the extra-cellular matrix, associated with a dynamic process of rotation around the anteroposterior axis. Here we show, by careful kinetic analysis of fat2 mutants, that neither basal planar polarization nor rotation is required during a first phase of follicle elongation. Conversely, a JAK-STAT signaling gradient from each follicle pole orients early elongation. JAK-STAT controls apical pulsatile contractions, and Myosin II activity inhibition affects both pulses and early elongation. Early elongation is associated with apical constriction at the poles and with oriented cell rearrangements, but without any visible planar cell polarization of the apical domain. Thus, a morphogen gradient can trigger tissue elongation through a control of cell pulsing and without a planar cell polarity requirement.

scholarly journals Cell non-autonomy amplifies disruption of neurulation by mosaic Vangl2 deletion in mice

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Gabriel L. Galea ◽  
Eirini Maniou ◽  
Timothy J. Edwards ◽  
Abigail R. Marshall ◽  
Ioakeim Ampartzidis ◽  
...  
Keyword(s):  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Myosin Ii ◽  
Apical Cell ◽  
Neural Tube Closure ◽  
Congenital Defects ◽  
Cell Cortex ◽  
Apical Constriction ◽  
Neuroepithelial Cells ◽  
Tube Closure

AbstractPost-zygotic mutations that generate tissue mosaicism are increasingly associated with severe congenital defects, including those arising from failed neural tube closure. Here we report that neural fold elevation during mouse spinal neurulation is vulnerable to deletion of the VANGL planar cell polarity protein 2 (Vangl2) gene in as few as 16% of neuroepithelial cells. Vangl2-deleted cells are typically dispersed throughout the neuroepithelium, and each non-autonomously prevents apical constriction by an average of five Vangl2-replete neighbours. This inhibition of apical constriction involves diminished myosin-II localisation on neighbour cell borders and shortening of basally-extending microtubule tails, which are known to facilitate apical constriction. Vangl2-deleted neuroepithelial cells themselves continue to apically constrict and preferentially recruit myosin-II to their apical cell cortex rather than to apical cap localisations. Such non-autonomous effects can explain how post-zygotic mutations affecting a minority of cells can cause catastrophic failure of morphogenesis leading to clinically important birth defects.

scholarly journals Actin and microtubules drive differential aspects of planar cell polarity in multiciliated cells

2011 ◽  
Vol 195 (1) ◽  
pp. 19-26 ◽  
Author(s):  
Michael E. Werner ◽  
Peter Hwang ◽  
Fawn Huisman ◽  
Peter Taborek ◽  
Clare C. Yu ◽  
...  
Keyword(s):  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Cell Polarization ◽  
Actin Dynamics ◽  
Cellular Organization ◽  
Cytoplasmic Microtubule ◽  
Local Coordination ◽  
Multiciliated Cells ◽  
Global Coordination ◽  
Microtubule Networks

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.

scholarly journals Functional plasticity of polarity proteins controls epithelial tissue architecture

2021 ◽  
Author(s):  
Cornélia Biehler ◽  
Katheryn E. Rothenberg ◽  
Alexandra Jetté ◽  
Hélori-Mael Gaudé ◽  
Rodrigo Fernandez-Gonzalez ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Domain Size ◽  
Cell Polarization ◽  
Epithelial Tissue ◽  
Tissue Architecture ◽  
Functional Plasticity ◽  
Apical Constriction ◽  
Dynamic Regulation ◽  
Cell Contractility ◽  
Apical Domain

AbstractThe Drosophila polarity protein Crumbs is essential for the establishment and growth of the apical domain in epithelial cells. Dynamic regulation of apical domain size is crucial for forming and maintaining complex epithelial structures such as tubes or acini. The protein Yurt limits the ability of Crumbs to promote apical membrane growth, thereby defining proper apical/basal membrane ratio that is essential for the functional architecture of epithelial cells. Here, we show that Yurt is not a general inhibitor of Crumbs, but rather hijacks Crumbs activity toward specific functions. In particular, Crumbs recruits Yurt to the apical domain to increase Myosin-dependent cortical tension while decreasing relative tissue viscosity. Yurt overexpression thus induces apical constriction in epithelial cells. The kinase aPKC phosphorylates Yurt, thereby dislodging the latter from the apical domain and releasing apical tension. In contrast, the kinase Pak1 promotes Yurt dephosphorylation through activation of the phosphatase PP2A. The Pak1–PP2A module thus opposes aPKC function and supports Yurt-induced apical constriction. Hence, the complex interplay between Yurt, aPKC, Pak1 and PP2A contributes to the functional plasticity of Crumbs. Overall, our data increase our understanding of how proteins sustaining epithelial cell polarization and Myosin-dependent cell contractility interact with one another to control epithelial tissue architecture.

scholarly journals LMO7-dependent apical constriction requires the binding of the Myosin heavy chain

2021 ◽  
Author(s):  
Miho Matsuda ◽  
Chih-Wen Chu ◽  
Sergei S Sokol
Keyword(s):  
Heavy Chain ◽  
Myosin Light Chain ◽  
Myosin Ii ◽  
Tube Formation ◽  
Epithelial Morphogenesis ◽  
Apical Constriction ◽  
Actomyosin Contractility ◽  
Apical Domain ◽  
Underlying Mechanisms ◽  
Muscle Myosin

The reduction of the apical domain, or apical constriction, is a process that occurs in a single cell or is coordinated in a group of cells in the epithelium. Coordinated apical constriction is particularly important when the epithelium is undergoing dynamic morphogenetic events such as furrow or tube formation. However, the underlying mechanisms remain incompletely understood. Here we show that Lim only protein 7 (Lmo7) is a novel activator of apical constriction in the Xenopus superficial ectoderm, which coordinates actomyosin contractility in a group of cells during epithelial morphogenesis. Like other apical constriction regulators, Lmo7 requires the activation of the Rho-Rock-Myosin II pathway to induce apical constriction. However, instead of increasing the phosphorylation of myosin light chain (MLC), Lmo7 binds muscle myosin II heavy chain A (NMIIA) and increases its association with actomyosin bundles at adherens junctions (AJs). Lmo7 overexpression modulates the subcellular distribution of Wtip, a tension marker at AJs, suggesting that Lmo7 generates mechanical forces at AJs. We propose that Lmo7 increases actomyosin contractility at AJs by promoting the formation of actomyosin bundles.

scholarly journals Cell polarity determinant Dlg1 facilitates epithelial invagination by promoting tissue-scale mechanical coordination

2021 ◽  
Author(s):  
Melisa Andrea Fuentes ◽  
Bing He
Keyword(s):  
Laser Ablation ◽  
Cell Polarity ◽  
Cortical Actin ◽  
Multilayered Structures ◽  
Directed Movement ◽  
Apical Constriction ◽  
Mechanical Coupling ◽  
Apical Domain ◽  
Epithelial Sheets ◽  
Fundamental Mechanism

Epithelial folding mediated by apical constriction serves as a fundamental mechanism to convert flat epithelial sheets into multilayered structures. It remains elusive whether additional mechanical inputs are required for folding mediated by apical constriction. Using Drosophila mesoderm invagination as a model, we identified an important role for the non-constricting, lateral mesodermal cells adjacent to the constriction domain ("flanking cells") in facilitating epithelial folding. We found that depletion of the basolateral determinant, Dlg1, disrupts the transition between apical constriction and invagination without affecting the rate of apical constriction. Strikingly, the observed delay in invagination is associated with ineffective apical myosin contractions in the flanking cells that lead to overstretching of their apical domain. The defects in the flanking cells impede ventral-directed movement of the lateral ectoderm, suggesting reduced mechanical coupling between tissues. Specifically disrupting the flanking cells in wildtype embryos by laser ablation or optogenetic depletion of cortical actin is sufficient to delay the apical constriction-to-invagination transition. Our findings indicate that effective mesoderm invagination requires intact flanking cells and suggest a role for tissue-scale mechanical coupling during epithelial folding.

scholarly journals Oxidized LDL/CD36 interaction induces loss of cell polarity and inhibits macrophage locomotion

2012 ◽  
Vol 23 (16) ◽  
pp. 3057-3068 ◽  
Author(s):  
Young Mi Park ◽  
Judith A. Drazba ◽  
Amit Vasanji ◽  
Thomas Egelhoff ◽  
Maria Febbraio ◽  
...  
Keyword(s):  
Cell Polarity ◽  
Oxidized Ldl ◽  
Oxidant Stress ◽  
Low Density Lipoprotein ◽  
Myosin Ii ◽  
Density Lipoprotein ◽  
Cell Polarization ◽  
Nucleotide Exchange ◽  
Intracellular Signals ◽  
Nucleotide Exchange Factor

Cell polarization is essential for migration and the exploratory function of leukocytes. However, the mechanism by which cells maintain polarity or how cells revert to the immobilized state by gaining cellular symmetry is not clear. Previously we showed that interaction between oxidized low-density lipoprotein (oxLDL) and CD36 inhibits macrophage migration; in the current study we tested the hypothesis that oxLDL/CD36-induced inhibition of migration is the result of intracellular signals that regulate cell polarity. Live cell imaging of macrophages showed that oxLDL actuated retraction of macrophage front end lamellipodia and induced loss of cell polarity. Cd36 null and macrophages null for Vav, a guanine nucleotide exchange factor (GEF), did not show this effect. These findings were caused by Rac-mediated inhibition of nonmuscle myosin II, a cell polarity determinant. OxLDL induced dephosphorylation of myosin regulatory light chain (MRLC) by increasing the activity of Rac. Six-thioguanine triphosphate (6-thio-GTP), which inhibits Vav-mediated activation of Rac, abrogated the effect of oxLDL. Activation of the Vav-Rac-myosin II pathway by oxidant stress may induce trapping of macrophages at sites of chronic inflammation such as atherosclerotic plaque.

scholarly journals STAT3 noncell-autonomously controls planar cell polarity during zebrafish convergence and extension

2004 ◽  
Vol 166 (7) ◽  
pp. 975-981 ◽  
Author(s):  
Chiemi Miyagi ◽  
Susumu Yamashita ◽  
Yusuke Ohba ◽  
Hisayoshi Yoshizaki ◽  
Michiyuki Matsuda ◽  
...  
Keyword(s):  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Cell Polarization ◽  
Rhoa Activity ◽  
Stat3 Signaling ◽  
Convergence And Extension ◽  
Pcp Signaling ◽  
Autonomous Activity ◽  
Rhoa Signaling ◽  
Transcription 3

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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