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.

The albino-deletion complex in the mouse defines genes necessary for development of embryonic and extraembryonic ectoderm

Development ◽  
1989 ◽  
Vol 105 (1) ◽  
pp. 175-182 ◽  
Author(s):  
L. Niswander ◽  
D. Yee ◽  
E.M. Rinchik ◽  
L.B. Russell ◽  
T. Magnuson
Keyword(s):  
Mouse Chromosome ◽  
Primitive Streak ◽  
Chromosome 7 ◽  
Complementation Analysis ◽  
Lethal Phenotype ◽  
Neural Axis ◽  
Embryological Analysis ◽  
Compound Heterozygotes

A detailed embryological analysis has been undertaken on embryos carrying the c4FR60Hd-, c5FR60Hg- or c2YPSj-albino deletions of mouse chromosome 7. Embryos homozygous for the c4FR60Hd deletion are abnormal at day 7.5 of gestation. The extraembryonic ectoderm does not develop, and primitive-streak formation and mesoderm production do not occur. In contrast, extensive development of the extraembryonic ectoderm, as well as mesoderm production, are observed in the c5FR60Hg- and c2YPSj-homozygous embryos. The mesoderm does not, however, organize into somites and the neural axis does not form. The embryos are grossly abnormal by day 8.5 of development. There are two other albino deletions (c6H and c11DSD) that are known to affect the embryo around the time of gastrulation (Niswander et al. 1988), and the lethal phenotype observed for the c4FR60Hd-homozygous embryos is similar to that described for c6H-homozygous embryos, whereas the c5FR60Hg- and c2YPSj-homozygous embryos display a phenotype that is similar to c11DSD-homozygous embryos. A detailed complementation analysis using these five deletions revealed that the c5FR60Hg, c2YPSj and c11DSD deletions could partially complement the phenotype produced by the c4FR60Hd and c6H deletions in any combination. Extensive development of the extraembryonic structures and production of mesoderm occurs in the compound heterozygotes. These results suggest that the distal breakpoints of the c5FR60Hg, c2YPSj and c11DSD deletions lie more proximal than the distal breakpoints of the c4FR60Hd and c6H deletions.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals GENETIC ANALYSIS OF THE ANTENNAPEDIA GENE COMPLEX (ANT-C) AND ADJACENT CHROMOSOMAL REGIONS OF DROSOPHILA MELANOGASTER. II. POLYTENE CHROMOSOME SEGMENTS 84A–84B1,2

Genetics ◽  
1980 ◽  
Vol 95 (2) ◽  
pp. 383-397
Author(s):  
R A Lewis ◽  
B T Wakimoto ◽  
R E Denell ◽  
T C Kaufman
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Analysis ◽  
Normal Development ◽  
Chromosome 3 ◽  
Gene Complex ◽  
Functional Sites ◽  
Complementation Groups ◽  
Chromosome Segments ◽  
New Alleles ◽  
New Mutations

ABSTRACT The existence of a gene complex in the proximal right arm of chromosome 3 of Drosophila melanogaster involved in the development of the head and thorax was originally suggested by the phenotypes of several dominant homoeotic mutations and their revertants. A screen for mutations utilizing Df(3R) AntpNS+R17 (proximally broken in salivary region 84B1,2) yielded, among 102 recovered mutations, 17 localized by deficiency mapping to the putative homoeotic cluster. These fell into four complementation groups, two of which were characterized by homoeotic phenotypes. To explore the limits of the Antennapedia gene complex (ANT-C) more proximally, a second screen has been undertaken utilizing Df(3R)Scr, a deficiency of 84A1-B1,2.——Of 2832 chromosomes screened, 21 bearing alterations localized to polytene interval 84A-84B1,2 have been recovered. Sixteen are recessive lethals, and five showing reduced viability display a visible phenotype in surviving individuals. Complementation and phenotypic analyses revealed four complementation groups proximal to those identified in the previous screen, including two new alleles of the recessive homoeotic mutation, proboscipedia (pb). Ten of the new mutations correspond to complementation groups defined previously in the Df(3R)AntpNS+R17 screen, four to the EbR11 group, two to the Scr group and four to the Antp group.——On the basis of the phenotypes of the 39 mutations localized to this region, plus their interactions with extant homoeotic mutations, we postulate that there are at least five functional sites comprising the ANT-C. Three have been demonstrated to he homoeotic in nature. The specific homoeotic transformations thus far observed suggest that these loci are critical for normal development of adult labial, maxillary and thoracic structures.

Rat embryonic ectoderm as renal isograft

Development ◽  
1986 ◽  
Vol 94 (1) ◽  
pp. 1-27
Author(s):  
Anton Švajger ◽  
Božica Levak-Švajger ◽  
Nikola Škreb
Keyword(s):  
Developmental Stage ◽  
Cell Population ◽  
Primitive Streak ◽  
Experimental Results ◽  
Current Concept ◽  
Embryonic Cells ◽  
Initial Cell ◽  
Mesoderm Formation ◽  
Distinct Features ◽  
Embryonic Ectoderm

Experimental results obtained many years ago revealed that during gastrulation (with the primitive streak and the mesoderm formation as distinct features) the early rodent embryo undergoes essential changes in its response to extrinsic teratogens (Russell & Russell, 1954; Wilson, 1954; Škreb, 1961; Škreb & Bijelić, 1962; Škreb & Frank, 1963). It has also been shown that the ultrastructural, histochemical and biosynthetic features of the embryo are subject to substantial changes during this period (Solter, Damjanov & Škreb, 1970, 1973; Dziadek & Adamson, 1978; Bode & Dziadek, 1979; Wartiovaara, Leivo & Vaheri, 1979; Jackson et al. 1981; Franke et al. 1982a, b). This suggests a restriction of developmental capacities (i.e. the loss of the capacity of regulation) in groups of embryonic cells at this developmental stage. According to the current concept, the initial cell population from which this restriction starts, resides within the embryonic ectoderm of the pregastrulation or preprimitive streak embryo (primitive or primary ectoderm).

scholarly journals The origin of mouse extraembryonic endoderm stem cell lines

2021 ◽  
Author(s):  
Jiangwei Lin
Keyword(s):  
Gene Expression ◽  
Cell Lines ◽  
Cell Lineage ◽  
Preimplantation Embryos ◽  
Visceral Endoderm ◽  
Primitive Endoderm ◽  
Cellular Origin ◽  
Extraembryonic Endoderm ◽  
Parietal Endoderm ◽  
Stem Cell Lines

Mouse extraembryonic endoderm stem (XEN) cell lines can be derived from preimplantation embryos (pre-XEN) and postimplantation embryos (post-XEN). XEN cells share a gene expression profile and cell lineage potential with primitive endoderm (PrE) blastocysts. However, the cellular origin of XEN cells in embryos remains unclear. Here, we report that post-XEN cell lines are derived both from the extraembryonic endoderm and epiblasts of postimplantation embryos and that pre-XEN cell lines are derived both from PrE and epiblasts of blastocysts. Our strategy consisted of deriving post-XEN cells from clumps of epiblasts, parietal endoderm (PE) and visceral endoderm (VE) and deriving pre-XEN cell lines from single PrE and single epiblasts of blastocysts. Thus, XEN cell lines in the mouse embryo originate not only from PrE and PrE-derived lineages but also from epiblast and epiblast-derived lineages of blastocysts and postimplantation embryos.

Plasminogen activator expression in F9 teratocarcinoma embryoid bodies and their endoderm derivatives

Development ◽  
1989 ◽  
Vol 106 (1) ◽  
pp. 195-201 ◽  
Author(s):  
K.R. Sabbag ◽  
J.E. Casanova ◽  
L.B. Grabel
Keyword(s):  
Plasminogen Activator ◽  
Plasminogen Activators ◽  
Culture Conditions ◽  
Embryoid Bodies ◽  
Tissue Type ◽  
Mrna Levels ◽  
Visceral Endoderm ◽  
Type Plasminogen Activator ◽  
Parietal Endoderm ◽  
F9 Teratocarcinoma

Plasminogen activators are believed to play an important role in tissue remodeling and cell migration. During mouse embryogenesis, visceral endoderm secretes urokinase-type plasminogen activator (uPA) whereas parietal endoderm secretes tissue-type plasminogen activator (tPA). Visceral endoderm from F9 embryoid bodies can transdifferentiate into parietal endoderm under the appropriate culture conditions. We have examined at the protein and mRNA levels the type of plasminogen activator expressed in whole embryoid bodies, visceral endoderm and its parietal endoderm derivatives. Our experiments show that the visceral endoderm on F9 embryoid bodies synthesizes and secretes substantial amounts of both tPA and uPA. In contrast, the parietal endoderm derived directly from the visceral endoderm secretes dramatically increased levels of tPA and decreases production of uPA to low or below detectable levels. These data support the finding that visceral endoderm can transdifferentiate to parietal endoderm. In addition, this transition provides an excellent model for studying the molecular basis of the coincident down- and upregulation of the two plasminogen activators as well as their potential function during embryogenesis.

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.

scholarly journals Mutations affecting development of the notochord in zebrafish

Development ◽  
1996 ◽  
Vol 123 (1) ◽  
pp. 117-128 ◽  
Author(s):  
D.L. Stemple ◽  
L. Solnica-Krezel ◽  
F. Zwartkruis ◽  
S.C. Neuhauss ◽  
A.F. Schier ◽  
...  
Keyword(s):  
Large Scale ◽  
Normal Development ◽  
Paraxial Mesoderm ◽  
Skeletal Element ◽  
Additional Insight ◽  
Genetic Pathway ◽  
Complementation Groups ◽  
Vertebrate Embryos ◽  
Insight Into

The notochord is critical for the normal development of vertebrate embryos. It serves both as the major skeletal element of the embryo and as a signaling source for the establishment of pattern within the neurectoderm, the paraxial mesoderm and other tissues. In a large-scale systematic screen of mutations affecting embryogenesis in zebrafish we identified 65 mutations that fall into 29 complementation groups, each leading to a defect in the formation and/or maintenance of the notochord. These mutations produce phenotypic abnormalities at numerous stages of notochord development, thereby establishing a phenotypic pathway, which in turn suggests a genetic pathway for the development of the notochord. Perturbations within adjacent tissues in mutant embryos further indicate the importance of notochord-derived signals for patterning within the embryo and suggest that these mutations will yield additional insight into the cues that regulate these patterning processes.

Potentiation by the lithium ion of morphogenetic responses to a Xenopus inducing factor

Development ◽  
1989 ◽  
Vol 105 (3) ◽  
pp. 549-558 ◽  
Author(s):  
J. Cooke ◽  
K. Symes ◽  
E.J. Smith
Keyword(s):  
Normal Development ◽  
Lithium Treatment ◽  
Lithium Ion ◽  
Specific Marker ◽  
Complete Suppression ◽  
Animal Pole ◽  
Low Concentrations ◽  
Mesoderm Formation

We have cultured explants of Xenopus blastular animal cap tissue from embryos that had received an earlier treatment with LiCl and from their untreated siblings, in various concentrations of XTC-cell-derived mesoderm-inducing factor (XTC-MIF, Smith, 1987; Smith et al. 1988). The pretreatment with lithium that we used transforms later morphogenesis in the whole embryo to give radialized body forms with anterior/dorsal levels of structure grossly over-represented. In addition, animal caps from ‘Li+’ embryos were allowed to develop without exposure to in vitro MIF (Li+ controls) and compared with normal uninduced control explants, and explants were made from normal early blastulae but given various initial treatments with LiCl in culture. The results confirm that the lithium ion itself will not induce mesoderm in competent, animal cap tissue of Xenopus. It does, however, enhance the responsiveness of this tissue to XTC-MIF, in a way that parallels its recently reported effect in the case of another mesoderm inducer of different character, bFGF (Slack et al. 1988). The effects observed are sufficient to imply that the altered body pattern that follows lithium treatment, in whole embryos, could be caused by modulation of the responses to an unaltered pattern of in situ inductive stimuli. We also observe evidence that appreciable inductive signals reach animal pole tissue beyond the limits of mesoderm formation in normal development. Relatively low concentrations of MIF prevent the development of an epidermis-specific marker in dissociated blastular animal cap cells (Symes et al. 1988). When such experiments are repeated in relation to the lithium pretreatment of embryos, such treatment is seen to have sensitized the cell population, so that the MIF concentration range that assures complete suppression of the marker is reduced. The results are discussed in relation to induction considered as pattern formation.

Sign in / Sign up

Export Citation Format

Share Document