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 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.

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.

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
Keyword(s):  
Neural Tube ◽  
Rho Gtpases ◽  
Cell Shape ◽  
Shape Change ◽  
Myosin Ii ◽  
Tube Formation ◽  
Neural Plate ◽  
Cell Shape Change ◽  
Neural Tube Formation

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.

scholarly journals Integrin binding and cell spreading on extracellular matrix act at different points in the cell cycle to promote hepatocyte growth.

1994 ◽  
Vol 5 (9) ◽  
pp. 967-975 ◽  
Author(s):  
L K Hansen ◽  
D J Mooney ◽  
J P Vacanti ◽  
D E Ingber
Keyword(s):  
Cell Cycle ◽  
Extracellular Matrix ◽  
Cell Shape ◽  
Time Course ◽  
Cell Spreading ◽  
S Phase ◽  
Similar Time ◽  
Cell Shape Changes ◽  
Hepatocyte Growth ◽  
Shape Changes

This study was undertaken to determine the importance of integrin binding and cell shape changes in the control of cell-cycle progression by extracellular matrix (ECM). Primary rat hepatocytes were cultured on ECM-coated dishes in serum-free medium with saturating amounts of growth factors (epidermal growth factor and insulin). Integrin binding and cell spreading were promoted in parallel by plating cells on dishes coated with fibronectin (FN). Integrin binding was separated from cell shape changes by culturing cells on dishes coated with a synthetic arg-gly-asp (RGD)-peptide that acts as an integrin ligand but does not support hepatocyte extension. Expression of early (junB) and late (ras) growth response genes and DNA synthesis were measured to determine whether these substrata induce G0-synchronized hepatocytes to reenter the growth cycle. Cells plated on FN exhibited transient increases in junB and ras gene expression (within 2 and 8 h after plating, respectively) and synchronous entry into S phase. Induction of junB and ras was observed over a similar time course in cells on RGD-coated dishes, however, these round cells did not enter S phase. The possibility that round cells on RGD were blocked in mid to late G1 was confirmed by the finding that when trypsinized and replated onto FN-coated dishes after 30 h of culture, they required a similar time (12-15 h) to reenter S phase as cells that had been spread and allowed to progress through G1 on FN. We have previously shown that hepatocytes remain viable and maintain high levels of liver-specific functions when cultured on these RGD-coated dishes. Thus, these results suggest that ECM acts at two different points in the cell cycle to regulate hepatocyte growth: first, by activating the G0/G1 transition via integrin binding and second, by promoting the G1/S phase transition and switching off the default differentiation program through mechanisms related to cell spreading.

scholarly journals Interplay between septin organization, cell cycle and cell shape in yeast

2005 ◽  
Vol 118 (8) ◽  
pp. 1617-1628 ◽  
Author(s):  
A. S. Gladfelter ◽  
L. Kozubowski ◽  
T. R. Zyla ◽  
D. J. Lew
Keyword(s):  
Cell Cycle ◽  
Cell Shape

scholarly journals Cell shape and contractility regulate ciliogenesis in cell cycle–arrested cells

2010 ◽  
Vol 191 (2) ◽  
pp. 303-312 ◽  
Author(s):  
Amandine Pitaval ◽  
Qingzong Tseng ◽  
Michel Bornens ◽  
Manuel Théry
Keyword(s):  
Cell Cycle ◽  
Primary Cilium ◽  
Network Architecture ◽  
Cell Shape ◽  
Individual Cell ◽  
Dorsal Surface ◽  
Ventral Surface ◽  
Control Individual ◽  
Cell Cycle Exit ◽  
Actin Network

In most lineages, cell cycle exit is correlated with the growth of a primary cilium. We analyzed cell cycle exit and ciliogenesis in human retinal cells and found that, contrary to the classical view, not all cells exiting the cell division cycle generate a primary cilium. Using adhesive micropatterns to control individual cell spreading, we demonstrate that cell spatial confinement is a major regulator of ciliogenesis. When spatially confined, cells assemble a contractile actin network along their ventral surface and a protrusive network along their dorsal surface. The nucleus–centrosome axis in confined cells is oriented toward the dorsal surface where the primary cilium is formed. In contrast, highly spread cells assemble mostly contractile actin bundles. The nucleus–centrosome axis of spread cells is oriented toward the ventral surface, where contractility prevented primary cilium growth. These results indicate that cell geometrical confinement affects cell polarity via the modulation of actin network architecture and thereby regulates basal body positioning and primary cilium growth.

scholarly journals A Complex of Two Centrosomal Proteins, CAP350 and FOP, Cooperates with EB1 in Microtubule Anchoring

2006 ◽  
Vol 17 (2) ◽  
pp. 634-644 ◽  
Author(s):  
Xiumin Yan ◽  
Robert Habedanck ◽  
Erich A. Nigg
Keyword(s):  
Cell Cycle ◽  
Mammalian Cells ◽  
Cell Shape ◽  
Terminal Domain ◽  
Centrosomal Proteins

The anchoring of microtubules (MTs) to subcellular structures is critical for cell shape, polarity, and motility. In mammalian cells, the centrosome is a prominent MT anchoring structure. A number of proteins, including ninein, p150Glued, and EB1, have been implicated in centrosomal MT anchoring, but the process is far from understood. Here we show that CAP350 and FOP (FGFR1 oncogene partner) form a centrosomal complex required for MT anchoring. We show that the C-terminal domain of CAP350 interacts directly with FOP and that both proteins localize to the centrosome throughout the cell cycle. FOP also binds to EB1 and is required for localizing EB1 to the centrosome. Depletion of either CAP350, FOP, or EB1 by siRNA causes loss of MT anchoring and profound disorganization of the MT network. These results have implications for the mechanisms underlying MT anchoring at the centrosome and they attribute a key MT anchoring function to two novel centrosomal proteins, CAP350 and FOP.

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