scholarly journals The Rap GTPase Activator Drosophila PDZ-GEF Regulates Cell Shape in Epithelial Migration and Morphogenesis

2007 ◽  
Vol 27 (22) ◽  
pp. 7966-7980 ◽  
Author(s):  
Benjamin Boettner ◽  
Linda Van Aelst
Keyword(s):  
Cell Shape ◽  
Developmental Stages ◽  
Myosin Ii ◽  
Wing Disc ◽  
Epithelial Morphogenesis ◽  
Dorsal Closure ◽  
Cell Contractility ◽  
Epithelial Migration ◽  
Epithelial Plasticity ◽  
Molecular Machinery

ABSTRACT Epithelial morphogenesis is characterized by an exquisite control of cell shape and position. Progression through dorsal closure in Drosophila gastrulation depends on the ability of Rap1 GTPase to signal through the adherens junctional multidomain protein Canoe. Here, we provide genetic evidence that epithelial Rap activation and Canoe effector usage are conferred by the Drosophila PDZ-GEF (dPDZ-GEF) exchange factor. We demonstrate that dPDZ-GEF/Rap/Canoe signaling modulates cell shape and apicolateral cell constriction in embryonic and wing disc epithelia. In dPDZ-GEF mutant embryos with strong dorsal closure defects, cells in the lateral ectoderm fail to properly elongate. Postembryonic dPDZ-GEF mutant cells generated in mosaic tissue display a striking extension of lateral cell perimeters in the proximity of junctional complexes, suggesting a loss of normal cell contractility. Furthermore, our data indicate that dPDZ-GEF signaling is linked to myosin II function. Both dPDZ-GEF and cno show strong genetic interactions with the myosin II-encoding gene, and myosin II distribution is severely perturbed in epithelia of both mutants. These findings provide the first insight into the molecular machinery targeted by Rap signaling to modulate epithelial plasticity. We propose that dPDZ-GEF-dependent signaling functions as a rheostat linking Rap activity to the regulation of cell shape in epithelial morphogenesis at different developmental stages.

scholarly journals Spectrin couples cell shape, cortical tension, and Hippo signaling in retinal epithelial morphogenesis

2020 ◽  
Vol 219 (4) ◽  
Author(s):  
Hua Deng ◽  
Limin Yang ◽  
Pei Wen ◽  
Huiyan Lei ◽  
Paul Blount ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Cell Shape ◽  
Myosin Ii ◽  
Epithelial Morphogenesis ◽  
Hippo Signaling ◽  
Membrane Domains ◽  
Apical Constriction ◽  
Cortical Tension ◽  
Mutant Cells ◽  
Apical Area

Although extracellular force has a profound effect on cell shape, cytoskeleton tension, and cell proliferation through the Hippo signaling effector Yki/YAP/TAZ, how intracellular force regulates these processes remains poorly understood. Here, we report an essential role for spectrin in specifying cell shape by transmitting intracellular actomyosin force to cell membrane. While activation of myosin II in Drosophila melanogaster pupal retina leads to increased cortical tension, apical constriction, and Yki-mediated hyperplasia, spectrin mutant cells, despite showing myosin II activation and Yki-mediated hyperplasia, paradoxically display decreased cortical tension and expanded apical area. Mechanistically, we show that spectrin is required for tethering cortical F-actin to cell membrane domains outside the adherens junctions (AJs). Thus, in the absence of spectrin, the weakened attachment of cortical F-actin to plasma membrane results in a failure to transmit actomyosin force to cell membrane, causing an expansion of apical surfaces. These results uncover an essential mechanism that couples cell shape, cortical tension, and Hippo signaling and highlight the importance of non–AJ membrane domains in dictating cell shape in tissue morphogenesis.

scholarly journals The Genes raw and ribbon Are Required for Proper Shape of Tubular Epithelial Tissues in Drosophila

Genetics ◽  
1997 ◽  
Vol 147 (1) ◽  
pp. 243-253 ◽  
Author(s):  
Joseph Jack ◽  
Guy Myette
Keyword(s):  
Embryonic Development ◽  
Salivary Glands ◽  
Cell Shape ◽  
Malpighian Tubules ◽  
Dorsal Closure ◽  
Epithelial Tissues ◽  
Cell Rearrangement

Abstract The products of two genes, raw and ribbon (rib), are required for the proper morphogenesis of a variety of tissues. Malpighian tubules mutant for raw or rib are wider and shorter than normal tubules, which are only two cells in circumference when they are fully formed. The mutations alter the shape of the tubules beginning early in their formation and block cell rearrangement late in development, which normally lengthens and narrows the tubes. Mutations of both genes affect a number of other tissues as well. Both genes are required for dorsal closure and retraction of the CNS during embryonic development. In addition, rib mutations block head involution, and broaden and shorten other tubular epithelia (salivary glands, tracheae, and hindgut) in much same manner as they alter the shape of the Malpighian tubules. In tissues in which the shape of cells can be observed readily, rib mutations alter cell shape, which probably causes the change in shape of the organs that are affected. In double mutants raw enhances the phenotypes of all the tissues that are affected by rib but unaffected by raw alone, indicating that raw is also active in these tissues.

Cell polarity and tissue patterning in plants

Development ◽  
1991 ◽  
Vol 113 (Supplement_1) ◽  
pp. 83-93 ◽  
Author(s):  
Tsvi Sachs
Keyword(s):  
Cell Polarity ◽  
Cell Shape ◽  
Auxin Transport ◽  
Developmental Stages ◽  
Important Determinant ◽  
Genetic System ◽  
Cell Patterning ◽  
Cell Polarization ◽  
Sources And Sinks ◽  
Tissue Patterning

Cell polarization is the specialization of developmental events along one orientation or one direction. Such polarization must be an early, essential stage of tissue patterning. The specification of orientation could not occur only at the level of the genetic system and it must express a coordination of events in many cells. There is a positive feedback relation between cell polarization and the transport of the known hormone auxin: polarity determines oriented auxin transport while transport itself induces both new and continued polarization. Since cell polarization increases gradually, this feedback leads to the canalization of transport – and of the associated cell differentiation – along defined strands of specialized cells. Recent work has shown that the same canalized flow can also be an important determinant of cell shape. In primordial, embryonic regions cell growth is oriented along the flow of auxin from the shoot towards the root. In later developmental stages the cells respond to the same flow by growing in girth, presumably adjusting the capacity of the tissues to the flow of signals. Finally, disrupted flow near wounds results in the development of relatively unorganized callus. Continued callus development appears to require the participation of the cells, as sources and sinks of auxin and other signals. The overall picture to emerge suggests that cell patterning can result from competition between cells acting as preferred channels, sources and sinks for developmental signals.

scholarly journals Myosin-dependent remodeling of adherens junctions protects junctions from Snail-dependent disassembly

2016 ◽  
Vol 212 (2) ◽  
pp. 219-229 ◽  
Author(s):  
Mo Weng ◽  
Eric Wieschaus
Keyword(s):  
Cell Shape ◽  
Adherens Junctions ◽  
Myosin Ii ◽  
Cell Junctions ◽  
Snail Expression ◽  
Quantitative Image ◽  
Early Expression ◽  
Temporally Correlated ◽  
Shape Changes

Although Snail is essential for disassembly of adherens junctions during epithelial–mesenchymal transitions (EMTs), loss of adherens junctions in Drosophila melanogaster gastrula is delayed until mesoderm is internalized, despite the early expression of Snail in that primordium. By combining live imaging and quantitative image analysis, we track the behavior of E-cadherin–rich junction clusters, demonstrating that in the early stages of gastrulation most subapical clusters in mesoderm not only persist, but move apically and enhance in density and total intensity. All three phenomena depend on myosin II and are temporally correlated with the pulses of actomyosin accumulation that drive initial cell shape changes during gastrulation. When contractile myosin is absent, the normal Snail expression in mesoderm, or ectopic Snail expression in ectoderm, is sufficient to drive early disassembly of junctions. In both cases, junctional disassembly can be blocked by simultaneous induction of myosin contractility. Our findings provide in vivo evidence for mechanosensitivity of cell–cell junctions and imply that myosin-mediated tension can prevent Snail-driven EMT.

The effects of the insect growth regulator fenoxycarb on Rhodnius prolixus (Insecta, Hemiptera) embryogenesis

1986 ◽  
Vol 64 (11) ◽  
pp. 2425-2429 ◽  
Author(s):  
Gregory Mitchell Kelly ◽  
Erwin Huebner
Keyword(s):  
Growth Regulator ◽  
Developmental Stages ◽  
Dose Range ◽  
Insect Growth Regulator ◽  
Rhodnius Prolixus ◽  
Dorsal Closure ◽  
Cellular Mechanisms ◽  
Insect Embryogenesis ◽  
Insect Growth ◽  
Experimental Tool

Embryonic development of the hemipteran Rhodnius prolixus is perturbed by fenoxycarb (Ro 13.5223, Dr. R. Maag Ltd.), a non-neurotoxic insect growth regulator. Degree of perturbation is dependent on dose applied and embryonic stage at application time. Day 5 embryos were the most sensitive over a broad dose range. Treatment on day 8 had little effect, with normal hatching occurring 1 week later. Three developmental stages were most sensitive to perturbation: katatrepsis, dorsal closure, and eclosion. Katatrepsis, which normally occurs 168 h postoviposition, was the stage most prominently affected, suggesting that fenoxycarb interferes with basic mechanisms underlying this morphogenetic movement. Dorsal closure was the second most sensistive stage, the defect being characterized by embryos failing to completely enclose the yolk. Embryos receiving very low doses successfully completed katatrepsis and dorsal closure but were unable to hatch. Results demonstrate that fenozycarb may be a useful experimental tool for examining the normal cellular mechanisms of insect embryogenesis.

scholarly journals Apical Accumulation of Rho in the Neural Plate Is Important for Neural Plate Cell Shape Change and Neural Tube Formation

2008 ◽  
Vol 19 (5) ◽  
pp. 2289-2299 ◽  
Author(s):  
Nagatoki Kinoshita ◽  
Noriaki Sasai ◽  
Kazuyo Misaki ◽  
Shigenobu Yonemura
Keyword(s):  
Neural Tube ◽  
Rho Gtpases ◽  
Cell Shape ◽  
Shape Change ◽  
Myosin Ii ◽  
Tube Formation ◽  
Neural Plate ◽  
Cell Shape Change ◽  
Neural Tube Formation

Although Rho-GTPases are well-known regulators of cytoskeletal reorganization, their in vivo distribution and physiological functions have remained elusive. In this study, we found marked apical accumulation of Rho in developing chick embryos undergoing folding of the neural plate during neural tube formation, with similar accumulation of activated myosin II. The timing of accumulation and biochemical activation of both Rho and myosin II was coincident with the dynamics of neural tube formation. Inhibition of Rho disrupted its apical accumulation and led to defects in neural tube formation, with abnormal morphology of the neural plate. Continuous activation of Rho also altered neural tube formation. These results indicate that correct spatiotemporal regulation of Rho is essential for neural tube morphogenesis. Furthermore, we found that a key morphogenetic signaling pathway, the Wnt/PCP pathway, was implicated in the apical accumulation of Rho and regulation of cell shape in the neural plate, suggesting that this signal may be the spatiotemporal regulator of Rho in neural tube formation.

scholarly journals Myosin IIB assembly state determines its mechanosensitive dynamics

2019 ◽  
Vol 218 (3) ◽  
pp. 895-908 ◽  
Author(s):  
Eric S. Schiffhauer ◽  
Yixin Ren ◽  
Vicente A. Iglesias ◽  
Priyanka Kothari ◽  
Pablo A. Iglesias ◽  
...  
Keyword(s):  
Mathematical Modeling ◽  
Cell Shape ◽  
Cellular Response ◽  
Myosin Ii ◽  
3T3 Cells ◽  
Dictyostelium Myosin ◽  
Highly Sensitive ◽  
Key Players ◽  
Nih 3T3 ◽  
Shape Changes

Dynamical cell shape changes require a highly sensitive cellular system that can respond to chemical and mechanical inputs. Myosin IIs are key players in the cell’s ability to react to mechanical inputs, demonstrating an ability to accumulate in response to applied stress. Here, we show that inputs that influence the ability of myosin II to assemble into filaments impact the ability of myosin to respond to stress in a predictable manner. Using mathematical modeling for Dictyostelium myosin II, we predict that myosin II mechanoresponsiveness will be biphasic with an optimum established by the percentage of myosin II assembled into bipolar filaments. In HeLa and NIH 3T3 cells, heavy chain phosphorylation of NMIIB by PKCζ, as well as expression of NMIIA, can control the ability of NMIIB to mechanorespond by influencing its assembly state. These data demonstrate that multiple inputs to the myosin II assembly state integrate at the level of myosin II to govern the cellular response to mechanical inputs.

scholarly journals A Drosophila homolog of the Rac- and Cdc42-activated serine/threonine kinase PAK is a potential focal adhesion and focal complex protein that colocalizes with dynamic actin structures.

1996 ◽  
Vol 16 (5) ◽  
pp. 1896-1908 ◽  
Author(s):  
N Harden ◽  
J Lee ◽  
H Y Loh ◽  
Y M Ong ◽  
I Tan ◽  
...  
Keyword(s):  
Focal Adhesion ◽  
Cell Shape ◽  
Focal Adhesions ◽  
Leading Edge ◽  
Epidermal Cells ◽  
Dorsal Closure ◽  
Serine Threonine Kinase ◽  
Threonine Kinase ◽  
Amino Terminal ◽  
Drosophila Homolog

Changes in cell morphology are essential in the development of a multicellular organism. The regulation of the cytoskeleton by the Rho subfamily of small GTP-binding proteins is an important determinant of cell shape. The Rho subfamily has been shown to participate in a variety of morphogenetic processes during Drosophila melanogaster development. We describe here a Drosophila homolog, DPAK, of the serine/threonine kinase PAK, a protein which is a target of the Rho subfamily proteins Rac and Cdc42. Rac, Cdc42, and PAK have previously been implicated in signaling by c-Jun amino-terminal kinases. DPAK bound to activated (GTP-bound) Drosophila Rac (DRacA) and Drosophila Cdc42. Similarities in the distributions of DPAK, integrin, and phosphotyrosine suggested an association of DPAK with focal adhesions and Cdc42- and Rac-induced focal adhesion-like focal complexes. DPAK was elevated in the leading edge of epidermal cells, whose morphological changes drive dorsal closure of the embryo. We have previously shown that the accumulation of cytoskeletal elements initiating cell shape changes in these cells could be inhibited by expression of a dominant-negative DRacA transgene. We show that leading-edge epidermal cells flanking segment borders, which express particularly large amounts of DPAK, undergo transient losses of cytoskeletal structures during dorsal closure. We propose that DPAK may be regulating the cytoskeleton through its association with focal adhesions and focal complexes and may be participating with DRacA in a c-Jun amino-terminal kinase signaling pathway recently demonstrated to be required for dorsal closure.

Second-Site Noncomplementation Identifies Genomic Regions Required for Drosophila Nonmuscle Myosin Function During Morphogenesis

Genetics ◽  
1998 ◽  
Vol 148 (4) ◽  
pp. 1845-1863
Author(s):  
Susan R Halsell ◽  
Daniel P Kiehart
Keyword(s):  
Cell Shape ◽  
Myosin Ii ◽  
Nonmuscle Myosin ◽  
Genetic Screens ◽  
Nonmuscle Myosin Ii ◽  
Cell Shape Changes ◽  
Genomic Regions ◽  
Shape Changes ◽  
Strong Interactors

Abstract Drosophila is an ideal metazoan model system for analyzing the role of nonmuscle myosin-II (henceforth, myosin) during development. In Drosophila, myosin function is required for cytokinesis and morphogenesis driven by cell migration and/or cell shape changes during oogenesis, embryogenesis, larval development and pupal metamorphosis. The mechanisms that regulate myosin function and the supramolecular structures into which myosin incorporates have not been systematically characterized. The genetic screens described here identify genomic regions that uncover loci that facilitate myosin function. The nonmuscle myosin heavy chain is encoded by a single locus, zipper. Contiguous chromosomal deficiencies that represent approximately 70% of the euchromatic genome were screened for genetic interactions with two recessive lethal alleles of zipper in a second-site noncomplementation assay for the malformed phenotype. Malformation in the adult leg reflects aberrations in cell shape changes driven by myosin-based contraction during leg morphogenesis. Of the 158 deficiencies tested, 47 behaved as second-site noncomplementors of zipper. Two of the deficiencies are strong interactors, 17 are intermediate and 28 are weak. Finer genetic mapping reveals that mutations in cytoplasmic tropomyosin and viking (collagen IV) behave as second-site noncomplementors of zipper during leg morphogenesis and that zipper function requires a previously uncharacterized locus, E3.10/J3.8, for leg morphogenesis and viability.

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