The Adhesive Properties and Expansion of the Chick Blastoderm

Development ◽  
1959 ◽  
Vol 7 (2) ◽  
pp. 146-164
Author(s):  
D. A. T. New

During the first 4 days of incubation the chick blastoderm expands to surround the yolk. Its expansion takes place over the inner surface of the vitelline membrane, and the edge of the blastoderm is firmly attached to this membrane. Little attention has been paid hitherto to the mechanism of this expansion, presumably because it lies outside the embryo proper. But many of the problems involved are of considerable interest, not only as they relate to development within cleidoic eggs, but also in connexion with more general questions affecting expansion of epithelia and the nature of cell surfaces. Blastoderm expansion has many points of similarity with the spreading of epithelia across wounds, and some of the factors involved may prove to be similar to those affecting the radiation of loose sheets of cells in tissue culture.

Development ◽  
1967 ◽  
Vol 17 (1) ◽  
pp. 195-212
Author(s):  
Ruth Bellairs ◽  
D. R. Bromham ◽  
C. C. Wylie

The area opaca of the chick blastoderm is generally regarded as being merely the primordium of the yolk sac. Thus it might be expected that during the early stages of development its role would be essentially to grow and to differentiate, rather than to exert any influence on the development of the area pellucida. Such a view would be supported by the fact that pieces of the area pellucida can differentiate in the absence of the area opaca if they are isolated on the chorioallantoic membrane (Rawles, 1936) or in vitro (de Haan, 1964). There are, however, reasons for enquiring whether the area opaca does exert some influence on the area pellucida. The first is that New (1959) has demonstrated that the blastoderm is normally under tension, and that this tension is produced by the peripheral cells of the area opaca which adhere to the inner surface of the vitelline membrane.


Development ◽  
1975 ◽  
Vol 34 (1) ◽  
pp. 265-277
Author(s):  
J. R. Downie

Since their discovery, cytoplasmic microtubules have been much studied in the context of cell movement and cell shape change. Much of the work has used drugs, particularly colchicine and its relatives, which break down microtubules — the so-called anti-tubulins. Colchicine inhibits the orientated movements of many cell types in vitro, and disrupts cell shape change in several morphogenetic situations. The investigation reported here used chick blastoderm expansion in New culture in an attempt to quantify the colchicine effect on orientated cell movement. However, although colchicine could halt blastoderm expansion entirely, a simple interpretation was not possible. (1) Colchicine at concentrations capable of blocking mitosis, and of disrupting all or most of the cytoplasmic microtubules of the cells studied, inhibited blastoderm expansion, often resulting in an overall retraction of the cell sheet. (2) Though blastoderm expansion does normally involve considerable cell proliferation, the colchicine effect could not be ascribed to a block on cell division since aminopterin, which stops cell division without affecting microtubules, did not inhibit expansion. (3) Blastoderm expansion is effected by the locomotion of a specialized band of edge cells at the blastoderm periphery. These are the only cells normally attached to the vitelline membrane — the substrate for expansion. When most of the blastoderm was excised, leaving the band of edge cells, and the cultures then treated with colchicine, expansion occurred normally. The colchicine effect on blastoderm expansion could not therefore be ascribed to a direct effect on the edge cells. (4) An alternative site of action of the drug is the remaining cells of the blastoderm. These normally become progressively flatter as expansion proceeds. If flattening in these cells is even partially dependent on their cytoplasmic microtubules, disruption of these microtubules might result in the inherent contractility of the cells resisting and eventually halting edge cell migration. That cell shape in these cells is dependent on microtubules was demonstrated by treating flat blastoderm fragments with colchicine. On incubation, the area occupied by these fragments decreased by 25–30 % more than controls. The significance of these results in the general context of orientated cell movements and cell shape determination is discussed, with particular emphasis on the analogous system of Fundulus epiboly.


1988 ◽  
Vol 89 (2) ◽  
pp. 207-216
Author(s):  
J.C. Jones

An analysis of the concanavalinA binding polypeptide components of bovine tongue epithelial desmosomes reveals that in addition to the known desmosomal glycoproteins of 100/115K (the ‘desmocollins’), 140K and 160/165K (‘desmoglein 1’) there is an uncharacterized glycoprotein of 125K (K = Mr × 10(−3). This latter polypeptide is immunologically distinct from known desmosomal glycoproteins, as determined by Western immunoblotting, but is recognized by an antibody preparation directed against the epithelial cell adhesion molecule E-cadherin. Moreover, the cadherin antibodies recognize a polypeptide present in bovine muzzle desmosomes that co-migrates with the 125K glycoprotein component of bovine tongue epithelial desmosomes. Upon treatment of bovine tongue desmosomes with a solution containing 9.5 M-urea, the 125K polypeptide becomes enriched in a urea-insoluble, membrane-enriched pelletable desmosomal fraction. Cadherin antibodies and antibodies directed against the 100/115K and 160/165K desmosomal glycoproteins generate similar immunofluorescence staining patterns in cryostat sections of bovine tongue epithelium. However, immunoelectron microscopic analysis of bovine tongue epithelium reveals that cadherin antibodies recognize components located both along the intercellular region of the desmosome and along nondesmosomal cell surfaces whereas antibodies directed against the 100/115K and the 160/165K desmosomal glycoproteins bind specifically to desmosomes. These results suggest that a cadherin-like glycoprotein component may play a role in the adhesive properties of the desmosomes of stratified squamous epithelia.


1969 ◽  
Vol 163 (2) ◽  
pp. 113-121 ◽  
Author(s):  
Ruth Bellairs ◽  
A. Boyde ◽  
Joan E. M. Heaysman

Parasitology ◽  
1979 ◽  
Vol 78 (2) ◽  
pp. 131-143 ◽  
Author(s):  
D. A. Wharton

SUMMARYThe ovary of Aspiculuris tetraptera has a prominent terminal cap cell. This is considered to be part of the ovarian epithelium. Oogonia detach from the short rachis and increase in size from 6 to 60 μm; accumulating hyaline granules, shell granules and glycogen. The hyaline granules persist in the egg cytoplasm after shell formation has been completed and are considered to be lipoprotein yolk. The shell granules contribute to the non-chitin fraction of the chitinous layer. A classification of the cytoplasmic inclusions of the nematode oocyte is proposed. Upon fertilization a vitelline membrane is formed which constitutes the vitelline layer of the egg-shell. The chitinous layer is secreted in the perivitelline space, between the vitelline layer and the egg oolemma. Upon completion of chitinous layer synthesis, the egg cytoplasm contracts away from its inner surface. The material of the lipid layer is secreted at the surface of the egg cytoplasm and adheres to the inner surface of the chitinous layer. During secretion of the chitinous and lipid layers by the egg cytoplasm, the uterine cells secrete the unit membrane-like external uterine layer and the crystalline internal uterine layer. A complex system of interconnecting spaces develops in the internal uterine layer. This system is open to the exterior via breaks in the external uterine layer. There is no direct involvement of the uterine cells in the formation of this structure.


1974 ◽  
Vol 62 (1) ◽  
pp. 198-214 ◽  
Author(s):  
Albert DiPasquale ◽  
Paul B. Bell

A variety of epithelial cells and fibroblasts fail to move over one another's upper surfaces in culture, resulting in monolayering. The failure of seeded fibroblasts to adhere to and spread on epithelial cell surfaces suggests that monolayering in culture is due to the lack of adhesion of the upper cell surface, at least of epithelial cells. Seeded fibroblasts and postmitotic, rounded fibroblasts likewise fail to spread on the upper surfaces of spread fibroblasts, suggesting that the inability of the upper cell surface to support spreading may be a general phenomenon. Inert particles and cell processes do not adhere directly to the upper cell surface. However, they can initiate adhesions to the surface at a cell's free margin, suggesting a variation of adhesive properties over a cell's surface.


1990 ◽  
Vol 139 (2) ◽  
pp. 407-416 ◽  
Author(s):  
James W. Lash ◽  
Edward Gosfield ◽  
David Ostrovsky ◽  
Ruth Bellairs

Development ◽  
1971 ◽  
Vol 26 (3) ◽  
pp. 623-635
Author(s):  
J. Roger Downie ◽  
Susan M. Pegrum

A band of cells forming the edge of the chick blastoderm, and attached to the vitelline membrane, causes the expansion of the blastoderm in the first few days of incubation by active migration across the vitelline membrane. The structure and organization of these cells was examined by light microscopy (both on whole mounts and sections) and transmission electron microscopy. The account presented differs markedly from previous descriptions of these cells. The band of cells at the blastoderm edge is an association, between 90 and 130 µm wide, of flattened, non-dividing cells forming a multilayer; some of these cells, and no other cells of the blastoderm, are attached to the vitelline membrane. Each attached cell has a thin flattened lamella, centrifugally oriented and underlapping the next cell distally, except (1) the most distal cell, whose lamella is thick and long, though tapering, and is not overlain by other cells; and (2) the most proximal attached cell which has a short centripetally oriented lamella, as well as a centrifugal underlapping one. The cells of the edge band not attached to the vitelline membrane also have flattened lamellae attached to the cells below; these lamellae are, however, unoriented. The cells of the edge band all have plentiful cortical filaments and cytoplasmic microtubules. Specialized plaques are involved in the attachment of edge band cells to the vitelline membrane. The form of this edge structure is compared with the outgrowth edge of a chick yolk sac epiblast explant cultured on vitelline membrane. It seems likely that the way the blastoderm edge cells are organized may explain their prodigious migratory activity.


Development ◽  
1953 ◽  
Vol 1 (4) ◽  
pp. 369-385
Author(s):  
Ruth Bellairs

The first of this series of papers (Bellairs, 1953) outlined the morphological changes occurring in the endoderm of the chick up to the stage of about ten pairs of somites; it also showed that the presumptive foregut area in the primitive streak stage blastoderm lies around the anterior end of the primitive streak, and at a slightly later stage around the head process. The present paper is concerned with the pattern of morphogenetic movements which occur in the endoderm during the early stages of foregut development. The technique involved the use of carbon marks upon the exposed endoderm of blastoderms grown dorsal side downwards in tissue culture by the watchglass method (Waddington, 1932; Bellairs, 1953). During the period of development investigated an expansion of the blastoderm as a whole took place over the plasma clot; the use of external reference points was therefore essential, although even with such aids it was not always possible to tell whether certain displacements of marked cells were in fact merely the expression of a general expansion or were due to a specific morphogenetic migration.


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