Developmental expression of the alpha receptor for platelet-derived growth factor, which is deleted in the embryonic lethal Patch mutation

Development ◽  
1992 ◽  
Vol 115 (1) ◽  
pp. 289-303 ◽  
Author(s):  
A. Orr-Urtreger ◽  
M.T. Bedford ◽  
M.S. Do ◽  
L. Eisenbach ◽  
P. Lonai
Keyword(s):  
Primitive Streak ◽  
Yolk Sac ◽  
Developmental Expression ◽  
Wild Type ◽  
Neural Tubes ◽  
Pdgfra Gene ◽  
Branchial Arches ◽  
Early Organogenesis ◽  
Visceral Yolk Sac ◽  
Parietal Endoderm

The alpha receptor of PDGF (Pdgfra) is expressed in primitive endoderm and mesoderm derivatives throughout embryogenesis. In the early primitive streak stage the gene is transcribed in the visceral and parietal endoderm. Later it is expressed in the presomitic mesoderm, yolk sac and amnion. During somitogenesis its transcription localizes to the heart and the somites. Subsequently, it is transcribed in the dermatome, the sclerotome, the developing limb and in various mesenchymal tissues of visceral organs. Its wild-type expression pattern correlates well with the phenotype of homozygous mutant Patch (Ph) embryos, where the Pdgfra gene is deleted. The Ph phenotype is first detectable at the primitive streak stage with convoluted and hypertrophic visceral yolk sac, deformed neural plate and disorganized or missing mesoderm. Most Ph/Ph embryos die before the 11th day of gestation. Those that survive till early organogenesis are very small, have hypertrophic yolk sacs, small and undifferentiated somites, convoluted neural tubes, large heart and pericardium, rudimentary limb buds and branchial arches. Our observations together suggest that the alpha PDGF receptor may be required for the normal development of visceral endoderm and mesoderm derivatives.

Cell fate, morphogenetic movement and population kinetics of embryonic endoderm at the time of germ layer formation in the mouse

Development ◽  
1987 ◽  
Vol 101 (3) ◽  
pp. 627-652 ◽  
Author(s):  
K.A. Lawson ◽  
R.A. Pedersen
Keyword(s):  
Cell Fate ◽  
Doubling Time ◽  
Primitive Streak ◽  
Yolk Sac ◽  
Population Doubling ◽  
Population Doubling Time ◽  
Germ Layer ◽  
Posterior Half ◽  
Visceral Yolk Sac

The fate of the embryonic endoderm (generally called visceral embryonic endoderm) of prestreak and early primitive streak stages of the mouse embryo was studied in vitro by microinjecting horseradish peroxidase into single axial endoderm cells of 6.7-day-old embryos and tracing the labelled descendants either through gastrulation (1 day of culture) or to early somite stages (2 days of culture). Descendants of endoderm cells from the anterior half of the axis were found at the extreme cranial end of the embryo after 1 day and in the visceral yolk sac endoderm after 2 days, i.e. they were displaced anteriorly and anterolaterally. Descendants of cells originating over and near the anterior end of the early primitive streak, i.e. posterior to the distal tip of the egg cylinder, were found after 1 day over the entire embryonic axis and after 2 days in the embryonic endoderm at the anterior intestinal portal, in the foregut, along the trunk and postnodally, as well as anteriorly and posteriorly in the visceral yolk sac. Endoderm covering the posterior half of the early primitive streak contributed to postnodal endoderm after 1 day (at the late streak stage) and mainly to posterior visceral yolk sac endoderm after 2 days. Clonal descendants of axial endoderm were located after 2 days either over the embryo or in the yolk sac; the few exceptions spanned the caudal end of the embryo and the posterior yolk sac. The clonal analysis also showed that the endoderm layer along the posterior half of the axis of prestreak- and early-streak-stage embryos is heterogeneous in its germ layer fate. Whereas the germ layer location of descendants from anterior sites did not differ after 1 day from that expected from the initial controls (approx. 90% exclusively in endoderm), only 62% of the successfully injected posterior sites resulted in labelled cells exclusively in endoderm; the remainder contributed partially or entirely to ectoderm and mesoderm. This loss from the endoderm layer was compensated by posterior-derived cells that remained in endoderm having more surviving descendants (8.4 h population doubling time) than did anterior-derived cells (10.5 h population doubling time). There was no indication of cell death at the prestreak and early streak stages; at least 93% of the cells were proliferating and more than half of the total axial population were in, or had completed, a third cell cycle after 22 h culture.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Histochemical differences in expression of X-linked glucose-6-phosphate dehydrogenase between ectoderm- and endoderm-derived embryonic and extra-embryonic tissues.

1991 ◽  
Vol 39 (5) ◽  
pp. 569-574 ◽  
Author(s):  
H Sobis ◽  
A Verstuyf ◽  
M Vandeputte
Keyword(s):  
X Chromosome ◽  
Yolk Sac ◽  
Wild Type ◽  
X Chromosomes ◽  
Tissue Sections ◽  
C3h Mice ◽  
Visceral Yolk Sac ◽  
Enzyme Deficient ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Derivatives Of

We examined the activity of X-linked glucose-6-phosphate dehydrogenase (G6PD) in concepti of the enzyme-deficient mutant and wild-type C3H mice. By using different crosses between the G6PD-deficient homozygous, heterozygous, or wild-type females and hemizygous or wild-type males, we confirmed the inactivation of one of the two X chromosomes in female concepti by a histochemical method. With this technique, a dual (G6PD + or -) cell population could be observed in the tissue sections. We demonstrate that the paternal X chromosome is inactivated in the endoderm of parietal and visceral yolk sac and in the trophoblast, whereas in the embryo and in the yolk sac mesoderm this inactivation is random. Our results confirm biochemical observations showing that only the maternal X chromosome is expressed in all derivatives of trophectoderm and primitive endoderm, whereas derivatives of the primitive ectoderm show random X chromosome expression.

Visualization of Antibody Transport in Rat Visceral Yolk-Sac Placenta

1982 ◽  
Vol 40 ◽  
pp. 246-247
Author(s):  
William P. Jollie
Keyword(s):  
Phosphate Buffer ◽  
Yolk Sac ◽  
Female Rats ◽  
Thin Sections ◽  
Visceral Yolk Sac ◽  
Antibody Complex ◽  
Cytochemical Reaction ◽  
Hind Foot ◽  
Antigen Antibody ◽  
Yolk Sac Placenta

A technique has been developed for visualizing antibody against horseradish peroxidase (HRP) in rat visceral yolk sac, the placental membrane across which passive immunity previously has been shown to be transferred from mother to young just prior to birth. Female rats were immunized by injecting both hind foot pads with 1 mg HRP emulsified in complete Freund's adjuvant. They were given a booster of 0.5mg HRP in 0.1 ml normal saline i.v. after one week, then bred and autopsied at selected stages of pregnancy, viz., 12, 1 7 and 22 days post coitum, receiving a second booster, injected as above, five days before autopsy. Yolk sacs were removed surgically and fixed immediately in 2% paraformaldehye, 1% glutaraldehye in 0.1 M phosphate buffer with 0.01% CaCl2 at pH 7.4, room temperature, for 3 hr, rinsed 3X in 0.1 M phosphate buffer plus 5% sucrose, then exposed to 1 mg HRP in 1 ml 0.1 M phosphate buffer at pH 7.4 for 1 hr. They were refixed in aldehydes, as above, for 1 5 min (to assure binding of antigen-antibody complex). Following buffer washes, the tissues were incubated in 3 mg diaminobenzidine tetrahydrochloride and 0.01% H2O2 in 0.05 M Tris-HCl buffer for 30 min. After brief buffer washes, they were postfixed in 2% OsO4. in phosphate buffer at pH 7.4, 4°C for 2 hr, dehydrated through a graded series of ethanols, and embedded in Durcupan. Thin sections were observed and photographed without contrast-enhancement with heavy metals. Cytochemical reaction product marked the site of HRP (i.e., antigen) which, in turn, was present only where it was bound with anti-HRP antibody.

Experimental yolk sac dysfunction as a model for studying nutritional disturbances in the embryo during early organogenesis

Teratology ◽  
1990 ◽  
Vol 41 (4) ◽  
pp. 405-413 ◽  
Author(s):  
R. L. Brent ◽  
D. A. Beckman ◽  
M. Jensen ◽  
T. R. Koszalka
Keyword(s):  
Yolk Sac ◽  
Early Organogenesis ◽  
Nutritional Disturbances

The activities of thiol proteases in the rat visceral yolk sac increase during late gestation

Placenta ◽  
1991 ◽  
Vol 12 (2) ◽  
pp. 143-151 ◽  
Author(s):  
John D. Grubb ◽  
Thomas R. Koszalk ◽  
Joseph J. Drabick ◽  
Robert M. Metrione
Keyword(s):  
Yolk Sac ◽  
Late Gestation ◽  
Visceral Yolk Sac ◽  
Thiol Proteases

Brachyury - a gene affecting mouse gastrulation and early organogenesis

Development ◽  
1992 ◽  
Vol 116 (Supplement) ◽  
pp. 157-165 ◽  
Author(s):  
R. S. P. Beddington ◽  
P. Rashbass ◽  
V. Wilson
Keyword(s):  
Es Cells ◽  
Embryonic Stem ◽  
Primitive Streak ◽  
Coat Colour ◽  
Es Cell ◽  
Wild Type ◽  
Mesoderm Cell ◽  
Rostrocaudal Axis

Mouse embryos that are homozygous for the Brachyury (T) deletion die at mid-gestation. They have prominent defects in the notochord, the allantois and the primitive streak. Expression of the T gene commences at the onset of gastrulation and is restricted to the primitive streak, mesoderm emerging from the streak, the head process and the notochord. Genetic evidence has suggested that there may be an increasing demand for T gene function along the rostrocaudal axis. Experiments reported here indicate that this may not be the case. Instead, the gradient in severity of the T defect may be caused by defective mesoderm cell movements, which result in a progressive accumulation of mesoderm cells near the primitive streak. Embryonic stem (ES) cells which are homozygous for the T deletion have been isolated and their differentiation in vitro and in vivo compared with that of heterozygous and wild-type ES cell lines. In +/+ ↔ T/T ES cell chimeras the Brachyury phenotype is not rescued by the presence of wild-type cells and high level chimeras show most of the features characteristic of intact T/T mutants. A few offspring from blastocysts injected with T/T ES cells have been born, several of which had greatly reduced or abnormal tails. However, little or no ES cell contribution was detectable in these animals, either as coat colour pigmentation or by isozyme analysis. Inspection of potential +/+ ↔ T/T ES cell chimeras on the 11th or 12th day of gestation, stages later than that at which intact T/T mutants die, revealed the presence of chimeras with caudal defects. These chimeras displayed a gradient of ES cell colonisation along the rostrocaudal axis with increased colonisation of caudal regions. In addition, the extent of chimerism in ectodermal tissues (which do not invaginate during gastrulation) tended to be higher than that in mesodermal tissues (which are derived from cells invaginating through the primitive streak). These results suggest that nascent mesoderm cells lacking the T gene are compromised in their ability to move away from the primitive streak. This indicates that one function of the T genemay be to regulate cell adhesion or cell motility properties in mesoderm cells. Wild-type cells in +/+ ↔ T/T chimeras appear to move normally to populate trunk and head mesoderm, suggesting that the reduced motility in T/T cells is a cell autonomous defect

Effect of yolk-sac antibody on rat embryos grown in culture

Development ◽  
1972 ◽  
Vol 27 (3) ◽  
pp. 543-553
Author(s):  
D. A. T. New ◽  
R. L. Brent
Keyword(s):  
Direct Contact ◽  
Culture Medium ◽  
Gamma Globulin ◽  
Yolk Sac ◽  
Amniotic Cavity ◽  
Pregnant Rats ◽  
Rat Embryos ◽  
Visceral Yolk Sac ◽  
Primary Action

Rat embryos, explanted with their embryonic membranes during the early stages of organogenesis ( days gestation), were grown in culture in roller tubes. Yolk-sac antibody (sheep anti rat yolk-sac gamma globulin), known to be teratogenic when injected into pregnant rats, was added to the culture medium. At concentrations of 0·1 mg/ml or more the antibody caused gross retardation of growth and differentiation. Injection of antibody into the amniotic cavity so that it had direct contact with the embryo, or between the amnion and yolk sac so that it was in contact with the mesodermal surface of the yolk sac, had little or no effect on development of the embryo or its membranes. These in vitro experiments indicate that yolk-sac antibody has an effect on development independent of any immunological reaction of the mother, and the primary action is probably on the visceral yolk-sac endoderm.

Study of yolk-sac endoderm organogenesis in the chick using a specific enzyme (cysteine lyase) as a marker of cell differentiation

Development ◽  
1973 ◽  
Vol 29 (1) ◽  
pp. 159-174
Author(s):  
Nelly Bennett
Keyword(s):  
Cell Differentiation ◽  
Blood Cells ◽  
Primitive Streak ◽  
Yolk Sac ◽  
Specific Enzyme ◽  
Cell Proliferation And Differentiation ◽  
Lyase Activity ◽  
Morphological Specialization

The detection of a specific enzyme (cysteine lyase) of the yolk-sac endoderm by a very sensitive method is employed to characterize cell differentiation during the early stages of endoderm organogenesis in the chick. The first cells to contain active cysteine lyase are found in the germ wall at the primitive streak stage. In vivo observations establish a relation between the morphological specialization and organization of endodermal cells, their loss of mitotic activity and the increase in cysteine lyase activity. They suggest an influence of the mesoderm on endoderm differentiation. In vitro experiments confirm the existence in the yolk-sac endoderm of an incompatibility between cell proliferation and differentiation, as well as the action of the mesoderm on both the structural organization of the endoblast and the appearance of cysteine lyase; this last action seems to be due mainly to blood cells; chicken and rabbit blood cells are equally active. The problems of the origin of the endoderm and of the interactions occurring during the organogenesis of the yolk-sac endoderm are discussed.

Sign in / Sign up

Export Citation Format

Share Document