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

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.

Author(s):  
Elena Gonzalez-Gobartt ◽  
José Blanco-Ameijeiras ◽  
Susana Usieto ◽  
Guillaume Allio ◽  
Bertrand Benazeraf ◽  
...  

SUMMARYBody axis elongation is a hallmark of the vertebrate embryo, involving the architectural remodelling of the tailbud. Although it is clear how bi-potential neuro-mesodermal progenitors (NMPs) contribute to embryo elongation, the dynamic events that lead to de novo lumen formation and that culminate in the formation of a 3-Dimensional, secondary neural tube from NMPs, are poorly understood. Here, we used in vivo imaging of the chicken embryo to show that cell intercalation downstream of TGF-beta/SMAD3 signalling is required for secondary neural tube formation. Our analysis describes the initial events in embryo elongation including lineage restriction, the epithelial-to-mesenchymal transition of NMPs, and the initiation of lumen formation. Importantly, we show that the resolution of a single, centrally positioned continuous lumen, which occurs through the intercalation of central cells, requires SMAD3 activity. We anticipate that these findings will be relevant to understand caudal, skin-covered neural tube defects, amongst the most frequent birth defects detected in humans.HIGHLIGHTS.- Initiation of the lumen formation follows the acquisition of neural identity and epithelial polarization..- Programmed cell death is not required for lumen resolution..- Resolution of a single central lumen requires cell intercalation, driven by Smad3 activity.- The outcome of central cell division preceding cell intercalation, varies along the cranio-caudal axis.


Development ◽  
1981 ◽  
Vol 61 (1) ◽  
pp. 35-49
Author(s):  
Eugenie C. Enslee ◽  
Lynn M. Riddiford

In the bug, Pyrrhocoris apterus, blastokinesis (a reversal of the position of the embryo within the egg) is seen to involve contraction of the serosa that is attached to the embryo's head. As the serosal cells change from squamous to columnar in the course of blastokinesis, a dense zone of microfilaments appears just under the apical surface. Many apical protrusions develop above this zone. After the embryo is in its final position the zone disappears and later the cells degenerate. Laterally, the serosal cells are connected by belt desmosornes, septate junctions and gap junctions. As blastokinesis progresses, more lateral surface is recruited below them from the original basal surface. Microtubules running parallel to the plasma membrane are seen near the apical microfilaments and along other surfaces of the cell. Secretory granules are evident both within serosal cells and along the apical surface, probably providing a lubricant for movement against the chorion. Yolk cells are common basal to the serosa, possibly mobilizing nutrients for it. This study of blastokinesis in Pyrrhocoris provides a dramatic example of cell shape change that is correlated with the appearance of microfilaments. In its details blastokinesis is comparable to morphogenetic events such as amphibian neural tube formation and ascidian metamorphosis.


Development ◽  
1987 ◽  
Vol 101 (4) ◽  
pp. 659-671 ◽  
Author(s):  
R.A. McCarthy ◽  
M.M. Burger

Laminin, a component of the embryonic sea urchin basal lamina, is recognized by monoclonal antibody BL1 (Mab BL1). Our results demonstrate that laminin is secreted into the blastcoel at the early blastula stage at a time when the blastomeres undergo a cell shape change and are organized into an epithelium. Laminin is present on the basal surfaces of ectodermal cells and is absent or reduced on migrating primary mesenchyme cells. Microinjection of a monoclonal antibody directed against laminin induces a morphological change in cell shape and a deformation of the embryonic epithelium. Investigation of selected stages of live embryos suggests that the distribution of laminin may be heterogeneous within the basal lamina during early development. The results implicate laminin as a mediator of cell shape change during early morphogenesis.


eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
SeYeon Chung ◽  
Sangjoon Kim ◽  
Deborah J Andrew

Apical constriction is a widely utilized cell shape change linked to folding, bending and invagination of polarized epithelia. It remains unclear how apical constriction is regulated spatiotemporally during tissue invagination and how this cellular process contributes to tube formation in different developmental contexts. Using Drosophila salivary gland (SG) invagination as a model, we show that regulation of folded gastrulation expression by the Fork head transcription factor is required for apicomedial accumulation of Rho kinase and non-muscle myosin II, which coordinate apical constriction. We demonstrate that neither loss of spatially coordinated apical constriction nor its complete blockage prevent internalization and tube formation, although such manipulations affect the geometry of invagination. When apical constriction is disrupted, compressing force generated by a tissue-level myosin cable contributes to SG invagination. We demonstrate that fully elongated polarized SGs can form outside the embryo, suggesting that tube formation and elongation are intrinsic properties of the SG.


Development ◽  
2002 ◽  
Vol 129 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Edwin M. Munro ◽  
Garrett Odell

The ascidian notochord forms through simultaneous invagination and convergent extension of a monolayer epithelial plate. Here we combine micromanipulation with time lapse and confocal microscopy to examine how notochord-intrinsic morphogenetic behaviors and interactions with surrounding tissues, determine these global patterns of movement. We show that notochord rudiments isolated at the 64-cell stage divide and become motile with normal timing; but, in the absence of interactions with non-notochordal tissues, they neither invaginate nor converge and extend. We find that notochord formation is robust in the sense that no particular neighboring tissue is required for notochord formation. Basal contact with either neural plate or anterior endoderm/lateral mesenchyme or posterior mesoderm are each alone sufficient to ensure that the notochord plate forms and extends a cylindrical rod. Surprisingly, the axis of convergent extension depends on the specific tissues that contact the notochord, as do other patterns of cell shape change, movement and tissue deformation that accompany notochord formation. We characterize one case in detail, namely, embryos lacking neural plates, in which a normal notochord forms but by an entirely different trajectory. Our results show ascidian notochord formation to be regulative in a fashion and to a degree never before appreciated. They suggest this regulative behavior depends on a complex interplay between morphogenetic tendencies intrinsic to the notochord plate and instructive and permissive interactions with surrounding tissues. We discuss mechanisms that could account for these data and what they imply about notochord morphogenesis and its evolution within the chordate phylum.


Development ◽  
1963 ◽  
Vol 11 (1) ◽  
pp. 155-166
Author(s):  
P. Malpoix ◽  
J. Quertier ◽  
J. Brachet

The inhibition by β-mercaptoethanol of morphogenesis in amphibians, freshwater hydra, planarians and regenerating tadpoles, has already been reported by one of us (Brachet, 1958, 1959a, b, c). The present work provides a closer analysis of the biological specificity of j8-mercaptoethanol with regard to the different movements which produce gastrulation in amphibians: invagination, epiboly, convergent stretching and ingression. The main result, obtained with Pleurodeles, was that gastrulation is completely inhibited by M/100 β-mercaptoethanol. Lower concentrations (M/300) permit more complete development, but the resulting embryos are abnormal. β-Mercaptoethanol interferes with neural tube formation, but has less effect on the development of the notochord and the mesodermal somites. It was further noted that, when embryos are treated at very early stages (1–2 cells, young blastulae), the blastocoele seems to collapse and the ectoblast of the animal pole is deeply puckered.


Sign in / Sign up

Export Citation Format

Share Document