Mechanisms of neurulation: traditional viewpoint and recent advances

Development ◽  
1990 ◽  
Vol 109 (2) ◽  
pp. 243-270 ◽  
Author(s):  
G.C. Schoenwolf ◽  
J.L. Smith
Keyword(s):  
Cell Shape ◽  
Molecular Mechanisms ◽  
Review Article ◽  
Neural Plate ◽  
Neuroepithelial Cell ◽  
Morphogenetic Movements ◽  
Cell Behaviors ◽  
Recent Advances ◽  
Future Challenges ◽  
Shape Changes

In this review article, the traditional viewpoint of how neurulation occurs is evaluated in light of recent advances. This has led to the formulation of the following fundamentals: (1) neurulation, specifically neural plate shaping and bending, is a multifactorial process resulting from forces both intrinsic and extrinsic to the neural plate; (2) neurulation is driven by both changes in neuroepithelial cell shape and other form-shaping events; and (3) forces for cell shape changes are generated by both the cytoskeleton and other factors. Several cell behaviors within the neural plate have been elucidated. Future challenges include identifying cell behaviors within non-neuroepithelial tissues, determining how intrinsic and extrinsic cell behaviors are orchestrated into coordinated morphogenetic movements and elucidating the molecular mechanisms underlying such behaviors.

Cell cycle and neuroepithelial cell shape during bending of the chick neural plate

1987 ◽  
Vol 218 (2) ◽  
pp. 196-206 ◽  
Author(s):  
Jodi L. Smith ◽  
Gary C. Schoenwolf
Keyword(s):  
Cell Cycle ◽  
Cell Shape ◽  
Neural Plate ◽  
Neuroepithelial Cell

scholarly journals broad controls leg imaginal disc morphogenesis in Drosophila via regulation of cell shape changes and remodeling of extracellular matrix

2019 ◽  
Author(s):  
Clinton Rice ◽  
Stuart Macdonald ◽  
Xiaochen Wang ◽  
Robert E Ward
Keyword(s):  
Extracellular Matrix ◽  
Transcription Factor ◽  
Drosophila Melanogaster ◽  
Cell Shape ◽  
Imaginal Disc ◽  
Molecular Mechanisms ◽  
Matrix Remodeling ◽  
Ecm Remodeling ◽  
Cell Shape Changes ◽  
Shape Changes

AbstractImaginal disc morphogenesis during metamorphosis in Drosophila melanogaster provides an excellent model to uncover molecular mechanisms by which hormonal signals effect physical changes during development. The broad (br) Z2 isoform encodes a transcription factor required for disc morphogenesis in response to 20-hydroxyecdysone, yet how it accomplishes this remains largely unknown. Here, we show that amorphic br5 mutant discs fail to remodel their basal extracellular matrix (ECM) after puparium formation and do not undergo necessary cell shape changes. RNA sequencing of wild type and mutant leg discs identified 717 genes differentially regulated by br; functional studies reveal that several are required for adult leg formation, particularly those involved in remodeling the ECM. Additionally, br Z2 expression is abruptly shut down at the onset of metamorphosis, and expressing it beyond this time results in failure of leg development during the late prepupal and pupal stages. Taken together, our results suggest that br Z2 is required to drive ECM remodeling, change cell shape, and maintain metabolic activity through the mid prepupal stage, but must be switched off to allow expression of pupation genes.Summary StatementThe Drosophila melanogaster ecdysone-responding transcription factor broad controls morphogenetic processes in leg imaginal discs during metamorphosis through regulation of genes involved in extracellular matrix remodeling, metabolism, and cell shape changes and rearrangements.

scholarly journals Recent advances in understanding the phenotypes of osteoarthritis

F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 2091 ◽  
Author(s):  
Ali Mobasheri ◽  
Simo Saarakkala ◽  
Mikko Finnilä ◽  
Morten A. Karsdal ◽  
Anne-Christine Bay-Jensen ◽  
...  
Keyword(s):  
Clinical Trials ◽  
Precision Medicine ◽  
Biochemical Markers ◽  
Molecular Mechanisms ◽  
Review Article ◽  
Clinical Phenotypes ◽  
Recent Advances ◽  
The People ◽  
Molecular Phenotypes

Recent research in the field of osteoarthritis (OA) has focused on understanding the underlying molecular and clinical phenotypes of the disease. This narrative review article focuses on recent advances in our understanding of the phenotypes of OA and proposes that the disease represents a diversity of clinical phenotypes that are underpinned by a number of molecular mechanisms, which may be shared by several phenotypes and targeted more specifically for therapeutic purposes. The clinical phenotypes of OA supposedly have different underlying etiologies and pathogenic pathways and they progress at different rates. Large OA population cohorts consist of a majority of patients whose disease progresses slowly and a minority of individuals whose disease may progress faster. The ability to identify the people with relatively rapidly progressing OA can transform clinical trials and enhance their efficiency. The identification, characterization, and classification of molecular phenotypes of rapidly progressing OA, which represent patients who may benefit most from intervention, could potentially serve as the basis for precision medicine for this disabling condition. Imaging and biochemical markers (biomarkers) are important diagnostic and research tools that can assist with this challenge.

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 Redundant type II cadherins define neuroepithelial cell states for cytoarchitectonic robustness

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Kou Hiraga ◽  
Yukiko U. Inoue ◽  
Junko Asami ◽  
Mayuko Hotta ◽  
Yuki Morimoto ◽  
...  
Keyword(s):  
Cell Shape ◽  
Individual Cell ◽  
Neural Plate ◽  
Single Type ◽  
Neuroepithelial Cell ◽  
Type Ii ◽  
Double Knockout ◽  
Determine Function ◽  
Neuroepithelial Cells ◽  
Shared Roles

Abstract Individual cell shape and integrity must precisely be orchestrated during morphogenesis. Here, we determine function of type II cadherins, Cdh6, Cdh8, and Cdh11, whose expression combinatorially demarcates the mouse neural plate/tube. While CRISPR/Cas9-based single type II cadherin mutants show no obvious phenotype, Cdh6/8 double knockout (DKO) mice develop intermingled forebrain/midbrain compartments as these two cadherins’ expression opposes at the nascent boundary. Cdh6/8/11 triple, Cdh6/8 or Cdh8/11 DKO mice further cause exencephaly just within the cranial region where mutated cadherins’ expression merges. In the Cdh8/11 DKO midbrain, we observe less-constricted apical actin meshwork, ventrally-directed spreading, and occasional hyperproliferation among dorsal neuroepithelial cells as origins for exencephaly. These results provide rigid evidence that, by conferring distinct adhesive codes to each cell, redundant type II cadherins serve essential and shared roles in compartmentalization and neurulation, both of which proceed under the robust control of the number, positioning, constriction, and fluidity of neuroepithelial cells.

scholarly journals Orchestrating morphogenesis: building the body plan by cell shape changes and movements

Development ◽  
2020 ◽  
Vol 147 (17) ◽  
pp. dev191049 ◽  
Author(s):  
Kia Z. Perez-Vale ◽  
Mark Peifer
Keyword(s):  
Cell Shape ◽  
Molecular Mechanisms ◽  
Fruit Fly ◽  
Body Plan ◽  
The Body ◽  
Collective Cell Migration ◽  
Convergent Extension ◽  
Apical Constriction ◽  
Cell Shape Changes ◽  
Shape Changes

ABSTRACTDuring embryonic development, a simple ball of cells re-shapes itself into the elaborate body plan of an animal. This requires dramatic cell shape changes and cell movements, powered by the contractile force generated by actin and myosin linked to the plasma membrane at cell-cell and cell-matrix junctions. Here, we review three morphogenetic events common to most animals: apical constriction, convergent extension and collective cell migration. Using the fruit fly Drosophila as an example, we discuss recent work that has revealed exciting new insights into the molecular mechanisms that allow cells to change shape and move without tearing tissues apart. We also point out parallel events at work in other animals, which suggest that the mechanisms underlying these morphogenetic processes are conserved.

scholarly journals The plastic cell: mechanical deformation of cells and tissues

Open Biology ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 210006
Author(s):  
Kelly Molnar ◽  
Michel Labouesse
Keyword(s):  
Cell Shape ◽  
Molecular Mechanisms ◽  
Magnetic Beads ◽  
Embryonic Cell ◽  
Permanent Cell ◽  
Experimental Approaches ◽  
Cell Shape Changes ◽  
Actin Remodelling ◽  
Fine Tune ◽  
Shape Changes

Epithelial cells possess the ability to change their shape in response to mechanical stress by remodelling their junctions and their cytoskeleton. This property lies at the heart of tissue morphogenesis in embryos. A key feature of embryonic cell shape changes is that they result from repeated mechanical inputs that make them partially irreversible at each step. Past work on cell rheology has rarely addressed how changes can become irreversible in a complex tissue. Here, we review new and exciting findings dissecting some of the physical principles and molecular mechanisms accounting for irreversible cell shape changes. We discuss concepts of mechanical ratchets and tension thresholds required to induce permanent cell deformations akin to mechanical plasticity. Work in different systems has highlighted the importance of actin remodelling and of E-cadherin endocytosis. We also list some novel experimental approaches to fine-tune mechanical tension, using optogenetics, magnetic beads or stretching of suspended epithelial tissues. Finally, we discuss some mathematical models that have been used to describe the quantitative aspects of accounting for mechanical cell plasticity and offer perspectives on this rapidly evolving field.

Neurulation in Xenopus laevis. An analysis and model based upon light and electron microscopy

Development ◽  
1970 ◽  
Vol 23 (2) ◽  
pp. 427-462
Author(s):  
Thomas E. Schroeder
Keyword(s):  
Electron Microscopy ◽  
Xenopus Laevis ◽  
Light And Electron Microscopy ◽  
Neural Plate ◽  
General Knowledge ◽  
Morphogenetic Movements ◽  
Model Based ◽  
Causal Mechanisms ◽  
Cytoplasmic Filaments ◽  
Shape Changes

It is a matter of general knowledge that neurulation, as it occurs in most chordate embryos, proceeds by longitudinal in-folding of the neural plate. Løvtrup (1965) ably described such morphogenetic movements as they occur in several neurulating amphibians. The mechanical causes of these movements are not clearly understood, however. In his review of the prominent theories of neurulation, Curtis (1967) points to their various inadequacies and concludes that ‘possibly the solution of this problem is to search for contractile movements in the cells involved in neurulation’ (p. 310). The present paper seeks to identify the causal mechanisms of neurulation in the African clawed toad Xenopus laevis. The study was originally undertaken specifically to test Cloney's (1966) prediction that the presumed contractility of neural plate cells is associated with the morphological presence of fine cytoplasmic filaments which actually constitute the molecular agents of contraction and cellular shape-changes.

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