The developmental analysis of an embryonic lethal (c 6H) in the mouse

Development ◽  
1976 ◽  
Vol 36 (2) ◽  
pp. 363-371
Author(s):  
Susan E. Lewis ◽  
Howard A. Turchin ◽  
Salome Gluecksohn-Waelsch
Keyword(s):  
Germ Layers ◽  
Development Study ◽  
Embryonic Lethal ◽  
Parietal Endoderm ◽  
Normal Differentiation ◽  
Developmental Analysis ◽  
Embryonic Ectoderm ◽  
Ectoplacental Cone

A development study of the effects of the cm allele at the albino locus has identified the c6H homozygote as an early postimplantation lethal. Homozygous c6H embryos can first be recognized at 6½–7 days of gestation by abnormalities of the ectoplacental cone and parietal endoderm. At 7½ days, mutant embryos appear severely retarded with obvious abnormalities in all germ layers. All c6H homozygotes are dead and resorbed by 8 days of development. It is proposed that the mutation interferes with the normal differentiation of the parietal endoderm, ectoplacental cone and extra-embryonic ectoderm of the egg cylinder.

Localization of trophoblast-defined surface antigens during early mouse embryogenesis

Development ◽  
1978 ◽  
Vol 43 (1) ◽  
pp. 147-156
Author(s):  
R. F. Searle ◽  
E. J. Jenkinson
Keyword(s):  
Rabbit Antiserum ◽  
Cell Populations ◽  
Electron Microscope Level ◽  
Cell Stage ◽  
Component Cell ◽  
Low Levels ◽  
Early Mouse ◽  
Post Implantation ◽  
Embryonic Ectoderm ◽  
Ectoplacental Cone

The binding pattern of a rabbit antiserum raised against mouse ectoplacental-cone trophoblast on component cell populations in the pre-implantation and early post-implantation mouse embryo has been examined at the electron-microscope level using an immunoperoxidase-labelling technique. Binding was not detectable on the 1-cell stage, appeared at low levels at the 8-cell stage ana was heavy on the trophectoderm and its trophoblast giant cell and extra-embryonic ectoderm descendants in the post-implantation embryo. In contrast, immunosurgically isolated 3½-day inner cell masses (ICM) showed only slight labelling, whilst ICM derivatives in the 7½-day embryo were unlabelled. The results indicate that the antiserum may be identifying a trophoblast-specific surface determinant(s), which appears with the differentiation of the trophectoderm and is maintained on some of the cell populations derived from this tissue at least until the early postimplantation stages.

scholarly journals Repression of Inappropriate Gene Expression in the Vertebrate Embryonic Ectoderm

Genes ◽  
2019 ◽  
Vol 10 (11) ◽  
pp. 895 ◽  
Author(s):  
Shoshana Reich ◽  
Daniel C. Weinstein
Keyword(s):  
Gene Expression ◽  
Xenopus Laevis ◽  
Cell Fate ◽  
Regulation Of Gene Expression ◽  
Model Organism ◽  
Cell Fate Determination ◽  
Vertebrate Development ◽  
Germ Layers ◽  
Inappropriate Gene Expression ◽  
Embryonic Ectoderm

During vertebrate embryogenesis, precise regulation of gene expression is crucial for proper cell fate determination. Much of what we know about vertebrate development has been gleaned from experiments performed on embryos of the amphibian Xenopus laevis; this review will focus primarily on studies of this model organism. An early critical step during vertebrate development is the formation of the three primary germ layers—ectoderm, mesoderm, and endoderm—which emerge during the process of gastrulation. While much attention has been focused on the induction of mesoderm and endoderm, it has become clear that differentiation of the ectoderm involves more than the simple absence of inductive cues; rather, it additionally requires the inhibition of mesendoderm-promoting genes. This review aims to summarize our current understanding of the various inhibitors of inappropriate gene expression in the presumptive ectoderm.

In vivo and in vitro development of mouse embryos homozygous for the embryonic lethal velvet coat (Ve) mutation

Development ◽  
1981 ◽  
Vol 66 (1) ◽  
pp. 43-55
Author(s):  
J. Rossant ◽  
K. M. Vijh
Keyword(s):  
Inner Cell Mass ◽  
Cell Mass ◽  
Giant Cells ◽  
Blastocyst Stage ◽  
Parietal Endoderm ◽  
Trophoblast Giant Cells ◽  
Vitro Development ◽  
Ectoplacental Cone

Embryos homozygous for the velvet coat mutation, Ve/Ve, were recognized at 6·5 days post coitum by the reduced size of the ectodermal portions of the egg cylinder and the loose, columnar nature of the overlying endoderm. Later in development ectoderm tissues were sometimes entirely absent. Abnormalities appeared in the ectoplacental cone at 8·5 days but trophoblast giant cells and parietal endoderm appeared unaffected. Homozygotes could not be unequivocally identified at 5·5 days nor at the blastocyst stage but were recognized in blastocyst outgrowths by poor development of the inner cell mass derivatives, It has previously been suggested that Ve may exert its action at the blastocyst stage by reducing the size of the inner cell mass, but no evidence for such a reduction was found. Most of the observations on Ve/Ve homozygotes are, however, consistent with the hypothesis that Ve exerts its action primarily on later primitive ectoderm development.

The albino deletion complex and early postimplantation survival in the mouse

Development ◽  
1988 ◽  
Vol 102 (1) ◽  
pp. 45-53 ◽  
Author(s):  
L. Niswander ◽  
D. Yee ◽  
E.M. Rinchik ◽  
L.B. Russell ◽  
T. Magnuson
Keyword(s):  
Normal Development ◽  
Tissue Type ◽  
Lethal Phenotype ◽  
Mesoderm Formation ◽  
Complementation Groups ◽  
Parietal Endoderm ◽  
Stem Cell Lines ◽  
Embryological Analysis ◽  
Embryonic Ectoderm ◽  
Homozygous Embryo

The albino deletion complex in the mouse represents 37 overlapping chromosomal deficiencies that have been arranged into at least twelve complementation groups. Many of the deletions cover regions of chromosome 7 that contain genes necessary for early embryonic development. The work reported here concentrates on two of these deletions (c6H, c11DSD), both of which were known to be lethal around the time of gastrulation when homozygous. A detailed embryological analysis has revealed distinct differences in the lethal phenotype associated with the c6H and c11DSD deletions. c6H homozygous embryos are grossly abnormal at day 7.5 of gestation, whereas c11DSD homozygous embryos appear abnormal at day 8.5 of gestation. There is no development of the extraembryonic ectoderm in c6H homozygotes, whereas extensive development of this tissue type occurs in c11DSD homozygotes. The visceral endoderm is abnormally shaped and the parietal endoderm appears to be overproduced in c6H homozygotes; these structures are not affected in c11DSD homozygotes. The embryonic ectoderm is runted in both types of embryo and it is not possible to obtain homozygous embryo-derived stem-cell lines for either deletion. Mesoderm formation occurs in the c11DSD but not in the c6H homozygotes. The c11DSD deletion chromosome complements the c6H chromosome in that the lethal phenotype of the compound heterozygote is similar to that of the c11DSD homozygote. These results suggest that a gene(s) necessary for normal development of the extraembryonic ectoderm is present in the c11DSD but deficient in the c6H deletion chromosome.

Tetraploid embryos rescue embryonic lethality caused by an additional maternally inherited X chromosome in the mouse

Development ◽  
1998 ◽  
Vol 125 (17) ◽  
pp. 3353-3363 ◽  
Author(s):  
Y. Goto ◽  
N. Takagi
Keyword(s):  
X Chromosome ◽  
High Frequency ◽  
Cell Lineage ◽  
Mouse Embryos ◽  
Primitive Endoderm ◽  
Parietal Endoderm ◽  
Maternal Imprinting ◽  
Early Lethality ◽  
Ectoplacental Cone ◽  
Chromosome Nondisjunction

Mouse embryos with an additional maternally inherited X chromosome, i.e., disomic for XM (DsXM), cease to grow early in development and have a deficient extraembryonic region. We hypothesized that the underdeveloped extraembryonic region is attributed to two copies of XM that escape inactivation due to maternal imprinting. To examine the validity of this hypothesis and throw more light on the significance of X chromosome dosage on cell differentiation, we generated DsXM(XMXMXP and XMXMY) embryos at a high frequency taking advantage of the elevated incidence of X chromosome nondisjunction in female mice heterozygous for two Robertsonian X-autosome translocations, Rb(X.2)2Ad and Rb(X.9)6H. Although two XM chromosomes seem to remain active in both trophectoderm and primitive endoderm, detailed histological examination showed that the polar trophectoderm derivatives (ectoplacental cone and extraembryonic ectoderm) are severely affected, but the primitive endoderm derivatives (visceral and parietal endoderm) are relatively unaffected. Successful rescue of DsXM embryos by aggregation with tetraploid embryos show that X chromosome inactivation occurred normally leaving one X active in epiblast derivatives. Thus, two copies of active XM chromosome in cells of the polar trophectoderm cell lineage seem to be the main cause of early lethality shown by DsXM embryos as a result of failure in formation of ectoplacental cone and extraembryonic ectoderm.

Histogenetic and neoplastic potential of different regions of the mouse embryonic egg cylinder

Development ◽  
1983 ◽  
Vol 75 (1) ◽  
pp. 189-204
Author(s):  
R. S. P. Beddington
Keyword(s):  
Embryonal Carcinoma ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cells ◽  
Germ Layers ◽  
Developmental Fate ◽  
Embryonic Ectoderm

The histogenetic and neoplastic potentials of defined regions of the 8th day mouse embryonic egg cylinder were examined following ectopic transfer to beneath the testis capsule. No differences in histogenetic potential were detected between anterior and posterior slices of the embryo, either when composed of all three germ layers or of embryonic ectoderm alone. Small anterior and distal fragments of embryonic ectoderm also produced similar histogenetic profiles, although posterior fragments failed to grow in this ectopic site. The histogenetic potential of anterior and distal fragments exceeded the developmental fate ascribed to these two regions in the embryo (Beddington, 1981). There was some evidence for regionalization with respect to neoplastic potential, anterior slices of the embryo giving rise to a higher incidence of embryonal carcinoma cells than posterior slices.

Growth Disturbance in Fetal Liver Hematopoiesis of Mll-Mutant Mice

Blood ◽  
1998 ◽  
Vol 92 (1) ◽  
pp. 108-117 ◽  
Author(s):  
Hideshi Yagi ◽  
Kenji Deguchi ◽  
Atsufumi Aono ◽  
Yoshihiko Tani ◽  
Tadamitsu Kishimoto ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fetal Liver ◽  
Homeobox Gene ◽  
Mutant Mice ◽  
Chromosomal Translocations ◽  
Homozygous Mutation ◽  
Growth Disturbance ◽  
Delayed Onset ◽  
Embryonic Lethal ◽  
Normal Differentiation

The MLL (ALL-1, HRX) gene is frequently involved in chromosomal translocations in acute leukemia and has homology with Drosophila trithorax, which controls homeobox gene expression and embryogenesis. To elucidate the function of Mll, we generated mice with a mutated Mll locus. Mice with a homozygous mutation were embryonic lethal and died at embryonic day 11.5 to 14.5, showing edematous bodies and petechiae. Histological examination revealed that hematopoietic cells were decreased in the liver of homozygous embryos, although they were composed of erythroid, myeloid, monocytic, and megakaryocytic cells with normal differentiation. Colony-forming assays using cells from fetal livers and yolk sacs showed that the number of colonies was markedly reduced and many of the colonies delayed to be recognized in Mllmu/mu embryos, although some of the colonies from Mllmu/mu embryos developed similarly with that from Mll+/+ and Mll+/mu embryos, suggesting the delayed onset of the proliferation of hematopoitic precursors. These data show that the hematopoietic precursors were greatly reduced in mutant mice, and suggest that Mll functions as a regulator of the growth of hematopoietic precursors.

Properties of extra-embryonic ectoderm isolated from postimplantation mouse embryos

Development ◽  
1977 ◽  
Vol 39 (1) ◽  
pp. 183-194
Author(s):  
J. Rossant ◽  
L. Ofer
Keyword(s):  
Mouse Embryo ◽  
Morphological Characteristics ◽  
Giant Cells ◽  
Mouse Embryos ◽  
Common Origin ◽  
Trophoblast Giant Cells ◽  
Embryonic Ectoderm ◽  
Ectoplacental Cone

Extra-embryonic ectoderm isolated from the mouse embryo as late as 8½ days post coitum can form cells with the morphological characteristics of trophoblast giant cells both in ectopic sites and in vitro. This similarity to the properties of ectoplacental cone tissue provides further support for the postulated common origin of both tissues from the trophectoderm of the blastocyst.

Investigation of the potency of cells from the postimplantation mouse embryo by blastocyst injection: a preliminary report

Development ◽  
1978 ◽  
Vol 48 (1) ◽  
pp. 239-247
Author(s):  
J. Rossant ◽  
R. L. Gardner ◽  
H. L. Alexandre
Keyword(s):  
Giant Cell ◽  
Mouse Embryo ◽  
Preliminary Report ◽  
Yolk Sac ◽  
Trophoblast Giant Cell ◽  
Visceral Endoderm ◽  
Visceral Yolk Sac ◽  
Cell Fractions ◽  
Embryonic Ectoderm ◽  
Ectoplacental Cone

Chimaeric conceptuses have been produced by injection of 5½- and 6½-day extra-embryonic ectoderm and 5½-day embryonic and extra-embryonic endoderm into 3½-day mouse blastocysts. Extra-embryonic ectoderm cells contributed only to the ectoplacental cone and/or trophoblast giant cell fractions, reflecting the probable trophectoderm origin of these cells. Proximal (visceral) endoderm cells overlying both the embryonic and extra-embryonic ectoderm contributed cells only to the endoderm of the visceral yolk sac, indicating that the definitive embryonic endoderm has not formed by 5½ days p.c.

scholarly journals GENETIC AND DEVELOPMENTAL ANALYSIS OF THE LOCUS vnd IN DROSOPHILA MELANOGASTER

Genetics ◽  
1983 ◽  
Vol 104 (3) ◽  
pp. 433-448
Author(s):  
Kalpana White ◽  
Normand L DeCelles ◽  
Thomas C Enlow
Keyword(s):  
Neural Development ◽  
Gene Function ◽  
Imaginal Disc ◽  
Thoracic Ganglion ◽  
Neural Cells ◽  
Genetic Mosaics ◽  
Hypomorphic Mutation ◽  
Embryonic Lethal ◽  
Developmental Analysis ◽  
New Alleles

ABSTRACT Genetic and developmental analysis of an X-linked vital locus vnd was undertaken. Embryos hemizygous for the original allele vnd did not hatch and exhibited a disorganized ventral nervous system (VNS). The mutation maps in the region 1B6-7 to 1B9-10, a subregion of an area previously shown to be essential to normal neural development. In this paper, we report isolation of five new alleles at the locus vnd. Genetic complementation analysis of all mutations at the vnd locus, with lethal alleles at adjacent loci, indicates that all lesions at the locus vnd affect only one vital gene function in the region. Four of the five alleles are embryonic lethal; one allele is subvital and behaves like an hypomorphic mutation. Hemizygous embryos for three of the four embryonic lethal alleles were inspected in histological sections; all exhibited disorganized VNS similar to the original allele. The developmental analysis in gynandromorphic genetic mosaics shows that (1) vnd  + gene function is not essential in most imaginal-disc cell derivatives, (2) only about 30% of the mosaic zygotes survive as adults, (3) mosaic zygotes with mutant tissue close to the head cuticle are least likely to survive, and (4) mutant tissue in the thoracic ganglion in the adult is not necessarily lethal. The mosaic data are consistent with the vnd  + gene function being necessary in neural cells derived from the anterioventral region of the blastoderm.

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