scholarly journals Downregulation of basal myosin‐ II is required for cell shape changes and tissue invagination

2018 ◽  
Vol 37 (23) ◽  
Author(s):  
Daniel Krueger ◽  
Pietro Tardivo ◽  
Congtin Nguyen ◽  
Stefano De Renzis
Keyword(s):  
Cell Shape ◽  
Myosin Ii ◽  
Cell Shape Changes ◽  
Shape Changes

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.

scholarly journals Myosin-II-mediated cell shape changes and cell intercalation contribute to primitive streak formation

2015 ◽  
Vol 17 (4) ◽  
pp. 397-408 ◽  
Author(s):  
Emil Rozbicki ◽  
Manli Chuai ◽  
Antti I. Karjalainen ◽  
Feifei Song ◽  
Helen M. Sang ◽  
...  
Keyword(s):  
Cell Shape ◽  
Myosin Ii ◽  
Primitive Streak ◽  
Cell Shape Changes ◽  
Cell Intercalation ◽  
Shape Changes

scholarly journals Viscoelastic dissipation stabilizes cell shape changes during tissue morphogenesis

2017 ◽  
Author(s):  
R Clément ◽  
C. Collinet ◽  
B. Dehapiot ◽  
T. Lecuit ◽  
P.-F. Lenne
Keyword(s):  
Optical Tweezers ◽  
Cell Shape ◽  
Myosin Ii ◽  
Force Generation ◽  
Tissue Morphogenesis ◽  
Cell Shape Changes ◽  
Cellular Forces ◽  
Transient Forces ◽  
Shape Changes

Tissue morphogenesis relies on the production of active cellular forces. Understanding how such forces are mechanically converted into cell shape changes is essential to our understanding of morphogenesis. Here we use Myosin II pulsatile activity during Drosophila embryogenesis to study how transient forces generate irreversible cell shape changes. Analyzing the dynamics of junction shortening and elongation resulting from Myosin II pulses, we find that long pulses yield less reversible deformations, typically a signature of dissipative mechanics. This is consistent with a simple viscoelastic description, which we use to model individual shortening and elongation events. The model predicts that dissipation typically occurs on the minute timescale, a timescale commensurate with that of force generation by Myosin II pulses. We test this estimate by applying time-controlled forces on junctions with optical tweezers. Our results argue that active junctional deformation is stabilized by dissipation. Hence, tissue morphogenesis requires coordination between force generation and dissipation.

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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