Epidermal metaplasia of proamnionic epithelium induced by dorsal skin dermis in the chick embryo

Development ◽  
1972 ◽  
Vol 27 (1) ◽  
pp. 199-213
Author(s):  
Takeo Mizuno

Proamnionic epithelium of the chick embryo cultivated directly on Wolff and Haffen's medium in the absence of mesenchymes fails to differentiate. Cultivation of the dorsal dermis of 6·5-day chick embryos in the absence of epithelium also results in lack of differentiation of dermal cells. When proamnionic epithelium taken from embryos before the 10-somite stage is cultivated combined with dorsal dermis of 6·5-day embryos for 6 days, the epithelium invariably undergoes metaplastic changes, forming stratified epidermis, sometimes with keratinized superficial layer. The underlying dermal cells are condensed and this often leads to the formation of feather germ-like structures. The competence of the epithelium for changing into the epidermis is gradually lost after the 10-somite stage, and the dorsal dermis from 8·5-day embryos is not very effective in inducing the epidermal metaplasia. Proamnionic epithelium cultivated on heat-killed dorsal dermis seems healthy but shows no sign of differentiation. Dorsal dermis combined with heat-killed proamnionic epithelium spreads and remains almost undifferentiated. These observations suggest that reciprocal induction mechanisms are involved in the epithelial and dermal differentiation. Cultivation of proamnionic epithelium with various heterologous mesenchymes or fragments of embryonic organs shows that this epithelium is only competent for epidermal differentiation when combined with dorsal dermis. When proamnion (proamnionic epithelium plus hypoblast) is directly combined with 6·5-day dorsal dermis it undergoes metaplastic changes. The same result is obtained when inverted (upside-down) proamnion is combined with the dermis. Hypoblast does not seem to affect the inductive interaction between the epithelium and the dorsal dermis.

Development ◽  
1987 ◽  
Vol 100 (3) ◽  
pp. 501-512 ◽  
Author(s):  
KUNIO KITAMURA

The dorsal skin of the chick embryo, in which feather germ forms, was found to synthesize two proteochondroitin sulphates, PCS-I and PCS-II and a proteoheparan sulphate, PHS. A monoclonal antibody (I3B9) was prepared against PCS-I, a higher molecular weight proteochondroitin sulphate. Distribution of PCS-I was immunohistochemically studied using I3B9. PCS-I was found in the epidermis, basement membrane and superficial dermis prior to formation of feather rudiments. As the feather rudiments formed, PCS-I was noted in a condensed area of dermal cells and in the basement membrane, while PCS-I decreased remarkably in the epidermal placode. The formation of feather buds resulted in a decrease in PCS-I in the region of dermal condensation and the basement membrane situated above this region. PCS-I was asymmetrically distributed in the feather filaments. The turnover of proteochondroitin sulphate was studied using autoradiography of [35S]sulphate. Proteochondroitin sulphate in the basement membrane and condensed dermis of the feather rudiments showed very slow turnover. On the other hand, the outgrowth of feather buds caused rapid turnover of proteochondroitin sulphate in the region of dermal condensation and basement membrane situated above this region. The mechanism for the uneven distribution of PCS-I during feather germ formation is discussed.


Development ◽  
1972 ◽  
Vol 28 (2) ◽  
pp. 313-341
Author(s):  
Par Annick Mauger

The role of somitic mesoderm in the development of dorsal plumage in chick embryos. I. Origin, regulation capacity and determination The role of somitic mesoderm in the development of the dorsal plumage has been studied in chick embryos. The operations were performed at 2–2·5 days of incubation. The replacement of a portion of somitic mesoderm by somitic mesoderm labelled with [3H]thymidine or obtained from Japanese quail embryos (whose nuclei bear distinctive specific markers) showed that cells originating from the dermatomes build up the dermis of the dorsal skin only. They do not migrate farther than approximately midway down the flank. Beyond this limit, dermal cells originate from the somatopleural mesoderm. The unsegmented somitic mesoderm is capable of extensive regulation, which leads to the development of a dorsal plumage, normal in the number and arrangement of its feathers according to the characteristic pattern of the spinal pteryla. Uni- or bilateral excision of segmented somitic mesoderm resulted in dorsal plumage deficiencies, the extent and frequency of which was related to the state of differentiation of the excised mesoderm. Thus, the excision of somites generally led to an incomplete spinal pteryla (absence of feather rows, apteria). However, the somitic mesoderm is still capable of regulation even though it has already undergone its differentiation into dermatome, myotome and sclerotome. These results show that somitic mesoderm retains its regulative capacity, even though it has already acquired its feather-forming determination. The replacement of unsegmented somitic mesoderm by various implants (agar, tantalum, gut, neural tube, somatopleural mesoderm), intended to block the regulation processes, abolished the differentiation of the spinal feathers on the operated side. In some cases, the implantation of somatopleural mesoderm resulted in the formation of a supernumerary tract. No tissue other than somitic mesoderm – not even the somatopleural mesoderm, which is normally in part feather-forming – is able to give rise to region-specific spinal pteryla dermis. The excision and replacement of somitic mesoderm prevented the differentiation of dense dermis, whereas these operations had no effect on the early histogenesis of the epidermis, with the formation of arches and anchor filaments.


Development ◽  
1970 ◽  
Vol 24 (3) ◽  
pp. 497-509
Author(s):  
Glenn C. Rosenquist

The origin of the prelung cells was determined by tracing the movements of [3H]thymidinelabelled grafts excised from medium-streak to 4-somite stage chick embryos and transplanted to the epiblast, streak, and endoderm-mesoderm of similarly staged recipient embryos. At the medium-streak stage the prelung endoderm cells are in the anterior third of the primitive streak; they shortly begin to migrate anteriorly and laterally into the endoderm layer. They are folded into the gut beginning at about the 4-somite stage, and begin to reach their definitive position in the ventrolateral gut wall at the 10- to 16-somite stage. At the ± 22-somite stage the prelung endoderm begins to burrow into the overlying splanchnic layer of mesoderm, pushing the prelung mesoderm ahead of it. At the medium-streak stage the prelung mesoderm is in the epiblast (dorsal) layer about half-way to the lateral margin of the area pellucida on either side of the streak, at a level about half-way between the anterior and posterior ends of the streak. From this position the prelung mesoderm migrates medially to the streak and is invaginated into the mesoderm layer at a position about half-way between the anterior and posterior ends of the streak. As a section of the dorsal mesentery, it migrates anteriorly and laterally from the streak into the splanchnic mesoderm lateral to the somites. From the head process stage to the early somite stages, the prelung mesoderm is located posterior to the prelung endoderm. The prelung mesoderm continues to migrate with the splanchnic mesoderm into the mesentery dorsal to the heart, where it invests the prelung endoderm after the 16- to 19-somite stage. Beginning at about the 22-somite stage, the prelung endoderm penetrates the prelung mesoderm and the bilateral bronchi are formed.


Development ◽  
1971 ◽  
Vol 25 (1) ◽  
pp. 97-113
Author(s):  
Glenn C. Rosenquist

The origin of the prehepatic cells was determined by tracing the movements of [3H]thymidine-labelled grafts excised from medium-streak to 4-somite stage chick embryos and transplanted to the epiblast, streak and endoderm-mesoderm layer of similarly staged recipient embryos. Although exact definition of prehepatic areas was not possible because of the small number of grafts placed at each developmental stage, the study showed in general that at the medium-streak stage, the prehepatic endoderm cells are in the anterior third of the primitive streak; they shortly begin to migrate anteriorly and laterally into the endoderm layer ventral to the precardiac areas of mesoderm. They are in the yolk-sac endoderm at the 2–4-somite stage, and by the 15–17-somite stage are clustered at the anterior intestinal portal. At the 26-somite to early limb-bud stages, the anterior and posterior liver diverticula have formed from these endoderm cells, and some of the branches of the diverticula may have reached the prehepatic mesenchyme, where the two tissues have begun to form cords and sinuses. At the medium-streak stage, the prehepatic mesoderm is located slightly more than halfway from the anterior to the posterior end of the primitive streak. From this position it migrates anteriorly and laterally into the lateral plate mesoderm, and from the head-process to the 2–4-somite stage it is situated posterior to the prehepatic endoderm and posterior and lateral to the heart-forming portion of the splanchnic layer. By the 15–17-somite stage the prehepatic mesoderm has reached a position in the splanchnic layer of mesoderm which forms the dorsolateral wall of the sinus venosus. By the 26-somite to early limb-bud stage the hepatic diverticula have joined with the hepatic mesenchyme to form the rudimentary cords and sinuses of the liver.


1977 ◽  
Vol 164 (3) ◽  
pp. 533-539 ◽  
Author(s):  
A Oikarinen

Collagen synthesis and the activities of prolyl hydroxylase, lysyl hydroxylase, collagen galactosyltransferase and collagen glucosyltransferase were studied in isolated chick-embryo tendon cells after the administration of cortisol acetate to the chick embryos. When the steroid was injected 1 day before isolation of the tendon cells, collagen synthesis was decreased, even though the enzyme activities were not changed. When cortisol acetate was given as repeated injections over a period of 4 days, both collagen synthesis and the enzyme activities decreased. The hydroxylase activities decreased even more than the two collagen glycosyltransferase activities, both in isolated cells and in whole chick embryos. The amount of prolyl hydroxylase protein diminished to the same extent as the enzyme activity, indicating that cortisol acetate inhibits enzyme synthesis. The inhibitory effect of cortisol acetate on collagen synthesis and on the enzyme activities was partially reversible in 3 days. Total protein synthesis was completely restored within this time. Only massive doses of cortisol acetate inhibited collagen synthesis in vitro. Additional experiments indicated that cortisol acetate did not decrease the rate of the enzyme reactions when added directly to the enzyme incubation mixtures. The results suggest that cortisol acetate decreases collagen synthesis both by its direct effect on collagen polypeptide-chain synthesis and by decreasing the activities of enzymes involved in post-translational modifications.


Development ◽  
1991 ◽  
Vol 111 (3) ◽  
pp. 699-713 ◽  
Author(s):  
X. Desbiens ◽  
C. Queva ◽  
T. Jaffredo ◽  
D. Stehelin ◽  
B. Vandenbunder

We have described the expression of three nuclear protooncogenes, c-myc, c-myb and c-ets-1 during feather morphogenesis in the chick embryo. In parallel with the expression patterns obtained by in situ hybridization, we have mapped the spatial distribution of S-phase cells by monitoring the incorporation of 5-bromodeoxyuridine. We do not detect c-myc or c-myb transcripts during the early stages when S-phase cells are scattered in the dermis and in the epidermis. Rather c-ets-1 transcripts are abundant in the dermal cells which divide and accumulate under the uniform epidermis. At the onset of the formation of the feather bud, cells within each rudiment cease DNA replicative activities and c-myc transcripts are detected both in the epidermis and in the underlying dermis. This expression precedes the reentry into the S phase. The transcription of c-myb, which has been previously tightly linked to hemopoietic cells is also detected in the developing skin. This expression is essentially located in proliferating epidermal cells on and after the beginning of feather outgrowth. As feather outgrowth proceeds, the distribution of c-myc and c-myb transcripts is restricted to the highly proliferating epidermis. In contrast c-ets-1 transcripts are never detected in the epidermis. During the later stages of skin morphogenesis, the transcription of c-ets-1 is restricted to the endothelial cells of blood vessels, as previously described. We suggest that the differential expression of these nuclear oncogenes reflects the activation of different mitotic controlling pathways during the development of the skin.


Development ◽  
1980 ◽  
Vol 59 (1) ◽  
pp. 59-69
Author(s):  
Kunio Kitamura

Changes in lectin activity during development of embryonic chick skin were studied. In the dorsal skin of the chick embryo in which feathers were formed, lectin activity first increased, during the period of dermal condensation, and then it decreased during the development of feathers. A similar change in lectin activity was also found in the anterior shank skin, the prospective scale region of the chick embryo. The embryonic cornea, in which no mesenchymal condensation took place, had lectin activity and did not show any developmental changes in lectin activity. Apteria regions of the dorsal skin, experimentally formed by treatment with hydrocortisone, gave low lectin activity. The lectin found in the embryonic skin showed specificity for lactose. The relationship found between lectin activity and dermal condensation in the embryonic chick skin is discussed.


Development ◽  
1959 ◽  
Vol 7 (1) ◽  
pp. 66-72
Author(s):  
L. Gwen Britt ◽  
Heinz Herrmann

The recent development of techniques originally devised by Waddington (1932) for the maintenance of the explanted chick embryo (Spratt, 1947; New, 1955; Wolff & Simon, 1955) has opened the possibility of determining quantitatively some parameters of the developmental processes occurring in embryonic tissues under these conditions. As a result of such measurements, protein accumulation in explanted embryos was found to be much smaller than in embryos developing in the egg. On the other hand, the progress of somite formation was found to take place at similar rates in embryos developing as explants or in situ (Herrmann & Schultz, 1958). The slow rate of protein accumulation in the explanted embryos made it seem desirable to investigate whether under some other conditions of explantation protein accumulation would approach more closely the rate of protein formation observed in the naturally developing embryo.


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