scholarly journals Neurulation in the Mexican salamander (Ambystoma mexicanum): a drug study and cell shape analysis of the epidermis and the neural plate

Development ◽  
1983 ◽  
Vol 74 (1) ◽  
pp. 275-295
Author(s):  
Rudolf B. Brun ◽  
John A. Garson
Keyword(s):  
Shape Analysis ◽  
Cell Shape ◽  
Neural Plate ◽  
Ambystoma Mexicanum ◽  
Drug Study ◽  
Semithin Sections ◽  
Cell Shape Changes ◽  
Fold Formation ◽  
Shape Changes

We analysed the neurulation movements in the Mexican salamander Ambystoma mexicanum. Embryos were exposed to colchicine or nocodazole prior to neural fold formation. Exposure to these drugs prevented the anterior neural folds from closing. Neurulation however proceeded normally in the posterior regions of the embryo. We were unable to find apically constricted cells in the neural plate of colchicine-blocked neurulae. Only rounded-up neural plate cells were present (semithin sections). This situation was typical in embryos exposed to colchicine prior to neural fold formation. Concentrations of colchicine up to 2·5 × 10−3 were not capable of blocking neurulation once the neural folds were formed. The wedge-shaped cells were present in similar numbers to those found in controls. We quantified the cell shape changes in the neural plate and in the epidermis in both controls and drug-arrested embryos. The comparison of these to classes of data shows that epidermal spreading is prevented by colchicine but only slightly affected by nocodazole. Embryos blocked in late neurulation by exposure to these drugs can resume neurulation following neural plate excision in nocodazole but not in colchicine. We conclude from this observation that the epidermis contributes to raising and closing of the neural folds. The presence of neural folds in absence of wedge-shaped cells in the neural plate is also taken as evidence that neurulation is not exclusively driven by forces generated in or acting on the neural plate. Our view on the concerted interplay of various embryonic components is illustrated in a summarizing diagram (Fig. 11).

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

scholarly journals Dependency relationships between IFT-dependent flagellum elongation and cell morphogenesis in Leishmania

Open Biology ◽  
2018 ◽  
Vol 8 (11) ◽  
pp. 180124 ◽  
Author(s):  
Jack Daniel Sunter ◽  
Flavia Moreira-Leite ◽  
Keith Gull
Keyword(s):  
Fluorescence Microscopy ◽  
Cell Shape ◽  
Electron Tomography ◽  
Intraflagellar Transport ◽  
Flagellar Pocket ◽  
Cell Morphogenesis ◽  
Multiple Functions ◽  
Cell Shape Changes ◽  
Shape Changes

Flagella have multiple functions that are associated with different axonemal structures. Motile flagella typically have a 9 + 2 arrangement of microtubules, whereas sensory flagella normally have a 9 + 0 arrangement. Leishmania exhibits both of these flagellum forms and differentiation between these two flagellum forms is associated with cytoskeletal and cell shape changes. We disrupted flagellum elongation in Leishmania by deleting the intraflagellar transport (IFT) protein IFT140 and examined the effects on cell morphogenesis. Δift140 cells have no external flagellum, having only a very short flagellum within the flagellar pocket. This short flagellum had a collapsed 9 + 0 (9v) axoneme configuration reminiscent of that in the amastigote and was not attached to the pocket membrane. Although amastigote-like changes occurred in the flagellar cytoskeleton, the cytoskeletal structures of Δift140 cells retained their promastigote configurations, as examined by fluorescence microscopy of tagged proteins and serial electron tomography. Thus, Leishmania promastigote cell morphogenesis does not depend on the formation of a long flagellum attached at the neck. Furthermore, our data show that disruption of the IFT system is sufficient to produce a switch from the 9 + 2 to the collapsed 9 + 0 (9v) axonemal structure, echoing the process that occurs during the promastigote to amastigote differentiation.

scholarly journals Tissue Flow Induces Cell Shape Changes During Organogenesis

2018 ◽  
Vol 115 (11) ◽  
pp. 2259-2270
Author(s):  
Gonca Erdemci-Tandogan ◽  
Madeline J. Clark ◽  
Jeffrey D. Amack ◽  
M. Lisa Manning
Keyword(s):  
Cell Shape ◽  
Cell Shape Changes ◽  
Shape Changes

scholarly journals Coordinated morphogenesis through tension-induced planar polarity

2017 ◽  
Author(s):  
Ghislain Gillard ◽  
Ophélie Nicolle ◽  
Thibault Brugières ◽  
Sylvain Prigent ◽  
Mathieu Pinot ◽  
...  
Keyword(s):  
Cell Shape ◽  
Muscle Contractions ◽  
Developmental Origins ◽  
Planar Polarity ◽  
C Elegans ◽  
Embryonic Tissues ◽  
Cell Shape Changes ◽  
Shape Changes

AbstractTissues from different developmental origins must interact to achieve coordinated morphogenesis at the level of a whole organism. C. elegans embryonic elongation is controlled by actomyosin dynamics which trigger cell shape changes in the epidermis and by muscle contractions, but how the two processes are coordinated is not known. We found that a tissue-wide tension generated by muscle contractions and relayed by tendon-like hemidesmosomes in the dorso-ventral epidermis is required to establish a planar polarity of the apical PAR module in the lateral epidermis. This planar polarized PAR module then controls actin planar organization, thus determining the orientation of cell shape changes and the elongation axis of the whole embryo. This trans-tissular mechanotransduction pathway thus contributes to coordinate the morphogenesis of three embryonic tissues.

scholarly journals Apical Constriction Reversal upon Mitotic Entry Underlies Different Morphogenetic Outcomes of Cell Division

2019 ◽  
Author(s):  
Clint S. Ko ◽  
Prateek Kalakuntla ◽  
Adam C. Martin
Keyword(s):  
Cell Division ◽  
Cell Shape ◽  
Mitotic Cell ◽  
Signal Interference ◽  
Apical Constriction ◽  
Mitotic Entry ◽  
Cell Divisions ◽  
Cell Shape Changes ◽  
Shape Changes ◽  
Mitotic Cells

AbstractDuring development, coordinated cell shape changes and cell divisions sculpt tissues. While these individual cell behaviors have been extensively studied, how cell shape changes and cell divisions that occur concurrently in epithelia influence tissue shape is less understood. We addressed this question in two contexts of the early Drosophila embryo: premature cell division during mesoderm invagination, and native ectodermal cell divisions with ectopic activation of apical contractility. Using quantitative live-cell imaging, we demonstrated that mitotic entry reverses apical contractility by interfering with medioapical RhoA signaling. While premature mitotic entry inhibits mesoderm invagination, which relies on apical constriction, mitotic entry in an artificially contractile ectoderm induced ectopic tissue invaginations. Ectopic invaginations resulted from medioapical myosin loss in neighboring mitotic cells. This myosin loss enabled non-mitotic cells to apically constrict through mitotic cell stretching. Thus, the spatial pattern of mitotic entry can differentially regulate tissue shape through signal interference between apical contractility and mitosis.

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