scholarly journals The Drosophila Ral GTPase Regulates Developmental Cell Shape Changes through the Jun NH2-terminal Kinase Pathway

1999 ◽  
Vol 146 (2) ◽  
pp. 361-372 ◽  
Author(s):  
Kazunobu Sawamoto ◽  
Per Winge ◽  
Shinya Koyama ◽  
Yuki Hirota ◽  
Chiharu Yamada ◽  
...  
Keyword(s):  
Cell Shape ◽  
Effector Proteins ◽  
Dominant Negative ◽  
Loss Of Function ◽  
Jnk Pathway ◽  
Cell Shape Changes ◽  
Ral Gtpase ◽  
Shape Changes ◽  
Constitutively Active

The Ral GTPase is activated by RalGDS, which is one of the effector proteins for Ras. Previous studies have suggested that Ral might function to regulate the cytoskeleton; however, its in vivo function is unknown. We have identified a Drosophila homologue of Ral that is widely expressed during embryogenesis and imaginal disc development. Two mutant Drosophila Ral (DRal) proteins, DRalG20V and DRalS25N, were generated and analyzed for nucleotide binding and GTPase activity. The biochemical analyses demonstrated that DRalG20V and DRalS25N act as constitutively active and dominant negative mutants, respectively. Overexpression of the wild-type DRal did not cause any visible phenotype, whereas DRalG20V and DRalS25N mutants caused defects in the development of various tissues including the cuticular surface, which is covered by parallel arrays of polarized structures such as hairs and sensory bristles. The dominant negative DRal protein caused defects in the development of hairs and bristles. These phenotypes were genetically suppressed by loss of function mutations of hemipterous and basket, encoding Drosophila Jun NH2-terminal kinase kinase (JNKK) and Jun NH2-terminal kinase (JNK), respectively. Expression of the constitutively active DRal protein caused defects in the process of dorsal closure during embryogenesis and inhibited the phosphorylation of JNK in cultured S2 cells. These results indicate that DRal regulates developmental cell shape changes through the JNK pathway.

scholarly journals Direct laser manipulation reveals the mechanics of cell contacts in vivo

2015 ◽  
Vol 112 (5) ◽  
pp. 1416-1421 ◽  
Author(s):  
Kapil Bambardekar ◽  
Raphaël Clément ◽  
Olivier Blanc ◽  
Claire Chardès ◽  
Pierre-François Lenne
Keyword(s):  
Cell Shape ◽  
Constitutive Law ◽  
Cell Junctions ◽  
Scale Model ◽  
Tissue Morphogenesis ◽  
Cell Contacts ◽  
Cell Shape Changes ◽  
Shape Changes ◽  
Cell Cell

Cell-generated forces produce a variety of tissue movements and tissue shape changes. The cytoskeletal elements that underlie these dynamics act at cell–cell and cell–ECM contacts to apply local forces on adhesive structures. In epithelia, force imbalance at cell contacts induces cell shape changes, such as apical constriction or polarized junction remodeling, driving tissue morphogenesis. The dynamics of these processes are well-characterized; however, the mechanical basis of cell shape changes is largely unknown because of a lack of mechanical measurements in vivo. We have developed an approach combining optical tweezers with light-sheet microscopy to probe the mechanical properties of epithelial cell junctions in the early Drosophila embryo. We show that optical trapping can efficiently deform cell–cell interfaces and measure tension at cell junctions, which is on the order of 100 pN. We show that tension at cell junctions equilibrates over a few seconds, a short timescale compared with the contractile events that drive morphogenetic movements. We also show that tension increases along cell interfaces during early tissue morphogenesis and becomes anisotropic as cells intercalate during germ-band extension. By performing pull-and-release experiments, we identify time-dependent properties of junctional mechanics consistent with a simple viscoelastic model. Integrating this constitutive law into a tissue-scale model, we predict quantitatively how local deformations propagate throughout the tissue.

scholarly journals Ectopic expression of constitutively activated Ral GTPase inhibits cell shape changes during Drosophila eye development

Oncogene ◽  
1999 ◽  
Vol 18 (11) ◽  
pp. 1967-1974 ◽  
Author(s):  
Kazunobu Sawamoto ◽  
Chiharu Yamada ◽  
Shosei Kishida ◽  
Yuki Hirota ◽  
Akiko Taguchi ◽  
...  
Keyword(s):  
Cell Shape ◽  
Eye Development ◽  
Ectopic Expression ◽  
Drosophila Eye ◽  
Cell Shape Changes ◽  
Ral Gtpase ◽  
Shape Changes

scholarly journals CDC42 and Rac1 control different actin-dependent processes in the Drosophila wing disc epithelium.

1995 ◽  
Vol 131 (1) ◽  
pp. 151-164 ◽  
Author(s):  
S Eaton ◽  
P Auvinen ◽  
L Luo ◽  
Y N Jan ◽  
K Simons
Keyword(s):  
Epithelial Cells ◽  
Cell Shape ◽  
Larval Instar ◽  
Cell Types ◽  
Wing Disc ◽  
Dominant Negative ◽  
The Third ◽  
Drosophila Wing ◽  
Cell Shape Changes ◽  
Shape Changes

Cdc42 and Rac1 are members of the rho family of small guanosinetriphosphatases and are required for a diverse set of cytoskeleton-membrane interactions in different cell types. Here we show that these two proteins contribute differently to the organization of epithelial cells in the Drosophila wing imaginal disc. Drac1 is required to assemble actin at adherens junctions. Failure of adherens junction actin assembly in Drac1 dominant-negative mutants is associated with increased cell death. Dcdc42, on the other hand, is required for processes that involve polarized cell shape changes during both pupal and larval development. In the third larval instar, Dcdc42 is required for apico-basal epithelial elongation. Whereas normal wing disc epithelial cells increase in height more than twofold during the third instar, cells that express a dominant-negative version of Dcdc42 remain short and are abnormally shaped. Dcdc42 localizes to both apical and basal regions of the cell during these events, and mediates elongation, at least in part, by effecting a reorganization of the basal actin cytoskeleton. These observations suggest that a common cdc42-based mechanism may govern polarized cell shape changes in a wide variety of cell types.

scholarly journals A genetic screen for temperature-sensitive morphogenesis-defectiveCaenorhabditis elegansmutants

2021 ◽  
Vol 11 (4) ◽  
Author(s):  
Molly C Jud ◽  
Josh Lowry ◽  
Thalia Padilla ◽  
Erin Clifford ◽  
Yuqi Yang ◽  
...  
Keyword(s):  
Cell Shape ◽  
The Body ◽  
Temperature Sensitive ◽  
Restrictive Temperature ◽  
Fundamental Biological Process ◽  
Embryonic Morphogenesis ◽  
Cell Shape Changes ◽  
Development Temperature ◽  
Multicellular Organisms ◽  
Shape Changes

AbstractMorphogenesis involves coordinated cell migrations and cell shape changes that generate tissues and organs, and organize the body plan. Cell adhesion and the cytoskeleton are important for executing morphogenesis, but their regulation remains poorly understood. As genes required for embryonic morphogenesis may have earlier roles in development, temperature-sensitive embryonic-lethal mutations are useful tools for investigating this process. From a collection of ∼200 such Caenorhabditis elegans mutants, we have identified 17 that have highly penetrant embryonic morphogenesis defects after upshifts from the permissive to the restrictive temperature, just prior to the cell shape changes that mediate elongation of the ovoid embryo into a vermiform larva. Using whole genome sequencing, we identified the causal mutations in seven affected genes. These include three genes that have roles in producing the extracellular matrix, which is known to affect the morphogenesis of epithelial tissues in multicellular organisms: the rib-1 and rib-2 genes encode glycosyltransferases, and the emb-9 gene encodes a collagen subunit. We also used live imaging to characterize epidermal cell shape dynamics in one mutant, or1219ts, and observed cell elongation defects during dorsal intercalation and ventral enclosure that may be responsible for the body elongation defects. These results indicate that our screen has identified factors that influence morphogenesis and provides a platform for advancing our understanding of this fundamental biological process.

Estradiol promotes cell shape changes and glial fibrillary acidic protein redistribution in hypothalamic astrocytes in vitro: A neuronal-mediated effect

Glia ◽  
1992 ◽  
Vol 6 (3) ◽  
pp. 180-187 ◽  
Author(s):  
Ignacio Torres-Aleman ◽  
Maria Teresa Rejas ◽  
Sebastian Pons ◽  
Luis Miguel Garcia-Segura
Keyword(s):  
Glial Fibrillary Acidic Protein ◽  
Cell Shape ◽  
Acidic Protein ◽  
Cell Shape Changes ◽  
Shape Changes
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