scholarly journals Disruption of the HNF-4 gene, expressed in visceral endoderm, leads to cell death in embryonic ectoderm and impaired gastrulation of mouse embryos.

1994 ◽  
Vol 8 (20) ◽  
pp. 2466-2477 ◽  
Author(s):  
W S Chen ◽  
K Manova ◽  
D C Weinstein ◽  
S A Duncan ◽  
A S Plump ◽  
...  
Development ◽  
1978 ◽  
Vol 43 (1) ◽  
pp. 289-313
Author(s):  
M. Dziadek ◽  
E. Adamson

The localization and synthesis of alphafoetoprotein (AFP) during mouse embryogenesis were studied by immunoperoxidase and by immunoprecipitation after radioactive labelling, using an antiserum prepared against AFP. AFP is first detectable in embryos on the 7th day of gestation (7th day embryos). In 7th and 8th day embryos AFP is confined to visceral (proximal) endoderm cells around the embryonic region of the egg cylinder. Visceral extra-embryonic and parietal (distal) endoderm cells do not contain AFP. By the 9th day of gestation AFP is also present in the extra-embryonic ectoderm, mesoderm and embryonic ectoderm cells around the three cavities of the embryo. These tissues do not synthesize AFP when cultured in isolation, but can adsorb AFP when it is added to the medium. On the 12th day of gestation AFP synthesis is confined to the endoderm layer of the visceral yolk sac. It is concluded that the ability to synthesize AFP is a property which is restricted to the visceral endoderm during early post-implantation development. The presence of AFP in other tissues of the embryo appears to be due to adsorption.


2000 ◽  
Vol 148 (3) ◽  
pp. 567-578 ◽  
Author(s):  
Joerg Huelsken ◽  
Regina Vogel ◽  
Volker Brinkmann ◽  
Bettina Erdmann ◽  
Carmen Birchmeier ◽  
...  

The anterior-posterior axis of the mouse embryo is defined before formation of the primitive streak, and axis specification and subsequent anterior development involves signaling from both embryonic ectoderm and visceral endoderm. Τhe Wnt signaling pathway is essential for various developmental processes, but a role in anterior-posterior axis formation in the mouse has not been previously established. β-Catenin is a central player in the Wnt pathway and in cadherin-mediated cell adhesion. We generated β-catenin–deficient mouse embryos and observed a defect in anterior-posterior axis formation at embryonic day 5.5, as visualized by the absence of Hex and Hesx1 and the mislocation of cerberus-like and Lim1 expression. Subsequently, no mesoderm and head structures are generated. Intercellular adhesion is maintained since plakoglobin substitutes for β-catenin. Our data demonstrate that β-catenin function is essential in anterior-posterior axis formation in the mouse, and experiments with chimeric embryos show that this function is required in the embryonic ectoderm.


Development ◽  
1978 ◽  
Vol 45 (1) ◽  
pp. 93-105
Author(s):  
Brigid Hogan ◽  
Rita Tilly

This paper describes the in vitro development of inner cell masses isolated immunosurgically from mouse blastocysts which had been collected on 3·5 days p.c. and then incubated for 24 h. The inner cell masses continue to grow in culture and develop through a series of stages with increasing complexity of internal organization. By day 1 all of the cultured ICMs have an outer layer of endoderm, and by day 3 some of them have two distinct kinds of inside cells; a columnar epithelial layer and a thin hemisphere of elongated cells. Later, mesodermal cells appear to delaminate from a limited region of the columnar layer, close to where it forms a junction with the thinner cells. By day 5, about 25% of the cultured ICMs have a striking resemblance to normal 7·5-day p.c. C3H embryos, with embryonic ectoderm, extra-embryonic ectoderm and chorion, embryonic and extra-embryonic mesoderm, and visceral endoderm. When mechanically disrupted and grown as attached clumps of cells in a tissue dish, these embryo-like structures give rise to trophoblast-like giant cells. These results suggest that the inner cell mass of 4·5-day p.c. blastocysts contains cells which can give rise to trophoblast derivates in culture.


Development ◽  
1981 ◽  
Vol 65 (Supplement) ◽  
pp. 269-287
Author(s):  
Michael H. L. Snow

The relationship between growth rate and regionalization of amphibian, bird and mammalian embryos is briefly reviewed. In contrast to the others, mammals start gastrulation with few cells but accelerate cell proliferation coincidentally. Experiments are described which demonstrate (1) autonomous development of pieces isolated surgically from such mouse embryos, and (2) an absence of regeneration or regulation. Since such embryos regulate completely after chemically induced random cell death it is postulated that these results reflect developmental determination and a resulting mosaicism that suggests development may have a clonal basis. Maps are drawn, allocating positions to various tissues in the embryo.


Development ◽  
1980 ◽  
Vol 55 (1) ◽  
pp. 33-51
Author(s):  
R. E. Poelmann

The shape of the embryonic ectoderm of early post-implantation mouse embryos changes greatly in the period of 6·2–7·3 days post coitum. The subcellular morphology of the embryonic ectoderm remains unchanged, except in the primitive-streak region. Cell kinetics differ between ectodermal regions. These differences may be related to the changes in the shape of the ectoderm. The increase in cell number in the lateral ectoderm (the prospective surface ectoderm) exceeds that in the frontal ectoderm (the future neurectoderm). This is not due to differences in the duration of the cell cycle. It can be explained, however, by the occurrence of different relative numbers of dividing and non-dividing cells. These numbers vary between the two regions. The percentage of non-dividing cells in the frontal ectoderm may reach 45, whereas in the lateral ectoderm this percentage is not higher than 15. Autoradiography in tritiated thymidine-treated embryos combined with the mitotic indices gave us all of the parameters necessary to present a model capable of clarifying the growth of the ectoderm during gastrulation, as well as the changes in the shape of the ectoderm.


Development ◽  
1992 ◽  
Vol 115 (1) ◽  
pp. 277-288 ◽  
Author(s):  
J.J. Lee ◽  
G. Radice ◽  
C.P. Perkins ◽  
F. Costantini

The H beta 58 transgenic mouse line carries a recessive insertional mutation that results in developmental abnormalities beginning at day 7.5 p.c. and embryonic arrest at about day 9.5. In this paper, we describe the characterization of a novel gene encoded at the H beta 58 locus, whose disruption appears to be responsible for the mutant phenotype. The wild-type H beta 58 gene encodes a single 2.7 kb mRNA during embryonic and fetal development, and in many adult somatic tissues. In the mutant locus, this transcription unit is split by the transgene insertion, and one of its coding exons is deleted. Consistent with the physical disruption of the gene, the level of the H beta 58 mRNA in heterozygous mutant mouse tissues was half the normal level, indicating that the mutant allele fails to encode a stable mRNA. In situ hybridization studies revealed that expression of the wild-type H beta 58 gene begins in the oocyte, and continues throughout pre- and post-implantation embryogenesis, despite the fact that homozygous mutant embryos develop successfully through the egg cylinder stage (day 6.5 p.c.). In the early post-implantation embryo, expression of the normal H beta 58 gene is relatively low in the embryonic ectoderm, the tissue displaying the earliest phenotypic effects of the mutation, and highest in the visceral endoderm. We therefore propose that the effects of the mutation on the embryonic ectoderm may be exerted indirectly, via the visceral endoderm. Sequence analysis of H beta 58 cDNA clones revealed no homology between the 38 × 10(3) M(r) H beta 58 protein and other known proteins. However, the H beta 58 gene displayed extremely strong conservation between mammals and birds (greater than 96% amino acid identity), although it appeared less conserved in amphibians and invertebrates.


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