Retinoic acid induces parietal endoderm but not primitive endoderm and visceral endoderm differentiation in F9 teratocarcinoma stem cells with a targeted deletion of the Rex-1 (Zfp-42) gene

2002 ◽  
Vol 195 (1-2) ◽  
pp. 119-133 ◽  
Author(s):  
James R Thompson ◽  
Lorraine J Gudas
Keyword(s):  
Stem Cells ◽  
Retinoic Acid ◽  
Visceral Endoderm ◽  
Primitive Endoderm ◽  
Targeted Deletion ◽  
Endoderm Differentiation ◽  
Parietal Endoderm ◽  
F9 Teratocarcinoma

scholarly journals Expression of fibroblast growth factor by F9 teratocarcinoma cells as a function of differentiation.

1989 ◽  
Vol 108 (6) ◽  
pp. 2467-2476 ◽  
Author(s):  
S J Braunhut ◽  
L J Gudas ◽  
T Kurokawa ◽  
J Sasse ◽  
P A D'Amore
Keyword(s):  
Stem Cells ◽  
Cdna Probe ◽  
Biologically Active ◽  
Endothelial Cell Proliferation ◽  
Fibroblast Growth ◽  
Basic Fgf ◽  
F9 Cells ◽  
Parietal Endoderm ◽  
F9 Teratocarcinoma ◽  
Proliferation Assays

F9 teratocarcinoma stem cells treated with retinoic acid (RA) and dibutyryl cAMP (but2 cAMP) differentiate into embryonic parietal endoderm. Using heparin-affinity chromatography, endothelial cell proliferation assays, immunoprecipitation, and Western analysis with antibodies specific for acidic and basic fibroblast growth factors (FGFs), we detected biologically active FGF in F9 cells only after differentiation. A bovine basic FGF cDNA probe hybridized to 2.2-kb mRNAs in both F9 stem and parietal endoderm cells and to a 3.8-kb mRNA in F9 stem cells. A genomic DNA probe for acidic FGF hybridized to a 5.8-6.0-kb mRNA in both F9 stem and parietal endoderm cells, and to a 6.0-6.3-kb mRNA only in parietal endoderm cells. Although these FGF mRNAs were present in the stem cells, we could find no evidence that F9 stem cells synthesized FGFs, whereas differentiated F9 cells synthesized both acidic and basic FGF-like proteins. We conclude that biologically active factors with properties characteristic of acidic and basic FGF are expressed by F9 parietal endoderm cells after differentiation. Differentiating embryonic parietal endoderm thus may serve as a source of FGF molecules in the developing blastocyst, where these factors appear to play a central role in subsequent embryogenesis.

Investigation of cell lineage and differentiation in the extraembryonic endoderm of the mouse embryo

Development ◽  
1982 ◽  
Vol 68 (1) ◽  
pp. 175-198
Author(s):  
R. L. Gardner
Keyword(s):  
Inner Cell Mass ◽  
Cell Mass ◽  
Cell Lineage ◽  
Early Embryo ◽  
Visceral Endoderm ◽  
Primitive Endoderm ◽  
Developmental Potential ◽  
Extraembryonic Endoderm ◽  
Parietal Endoderm ◽  
Endodermal Cells

The technique of injecting genetically labelled cells into blastocysts was used in an attempt to determine whether the parietal and visceral endoderm originate from the same or different cell populations in the early embryo. When the developmental potential of 5th day primitive ectoderm and primitive endoderm cells was compared thus, only the latter were found to colonize the extraembryonic endoderm. Furthermore, single primitive endoderm cells yielded unequivocal colonization of both the parietal and the visceral endoderm in a proportion of chimaeras. However, in the majority of primitive endodermal chimaeras, donor cells were detected in the parietal endoderm only, cases of exclusively visceral colonization being rare. Visceral endoderm cells from 6th and 7th day post-implantation embryos also exhibited a striking tendency to contribute exclusively to the parietal endoderm following blastocyst injection. The above findings lend no support to a recent proposal that parietal and visceral endoderm are derived from different populations of inner cell mass cells. Rather, they suggest that the two extraembryonic endoderm layers originate from a common pool of primitive endoderm cells whose direction of differentiation depends on their interactions with non-endodermal cells.

scholarly journals Retinoic Acid Receptor Isotype Specificity in F9 Teratocarcinoma Stem Cells Results from the Differential Recruitment of Coregulators to Retinoic Acid Response Elements

2007 ◽  
Vol 282 (46) ◽  
pp. 33421-33434 ◽  
Author(s):  
Robert F. Gillespie ◽  
Lorraine J. Gudas
Keyword(s):  
Stem Cells ◽  
Retinoic Acid ◽  
Target Genes ◽  
Retinoic Acid Receptor ◽  
Polycomb Group ◽  
Polycomb Group Protein ◽  
Response Elements ◽  
Acid Receptor ◽  
Group Protein ◽  
F9 Teratocarcinoma

The retinoic acid receptor (RAR) α, β2, and γ isotypes each regulate specific subsets of target genes in F9 teratocarcinoma stem cells. We used chromatin immunoprecipitation assays to monitor the association of RARγ, retinoic X receptor (RXR) α, and coregulators with the RARβ2, Hoxa1, and Cyp26A1 retinoic acid response elements (RAREs) in F9 wild type and RARα, -β2, and -γ null cells. Additionally we quantitatively monitored expression of the corresponding mRNAs. We demonstrated that the association of RARγ and/or RXRα with a RARE was not sufficient for retinoic acid (RA)-mediated transcription of the corresponding target gene. However, the ability of RARγ and/or RXRα to recruit pCIP (AIB1/ACTR/RAC-3/TRAM-1/SRC-3) and p300 to a RARE did correlate with RA-associated transcription of target mRNAs. Therefore, the specific functions of the RAR isotypes do not manifest at the level of their DNA binding but rather from a differential ability to recruit specific components of the transcriptional machinery. We also demonstrated that RA-mediated displacement of the polycomb group protein SUZ12 from a RARE was inhibited in the absence of RARγ. Thus, transcriptional components of the RAR signaling pathway are specifically required for displacement of SUZ12 from RAREs during RA-mediated differentiation of F9 cells.

scholarly journals Frizzled gene expression and negative regulation of canonical WNT–β-catenin signaling in mouse F9 teratocarcinoma cells

2017 ◽  
Vol 95 (2) ◽  
pp. 251-262 ◽  
Author(s):  
Gregory Golenia ◽  
Mohamed I. Gatie ◽  
Gregory M. Kelly
Keyword(s):  
Feedback Loop ◽  
Negative Regulation ◽  
Negative Feedback Loop ◽  
Primitive Endoderm ◽  
F9 Cells ◽  
Knock Down ◽  
Teratocarcinoma Cells ◽  
Parietal Endoderm ◽  
F9 Teratocarcinoma ◽  
Canonical Wnt

Mouse F9 cells differentiate into primitive endoderm (PrE) following the activation of the canonical WNT–β-catenin pathway. The upregulation of Wnt6 and activation of β-catenin–TCF–LEF-dependent transcription is known to accompany differentiation, but the Frizzled (FZD) receptor responsible for transducing the WNT6 signal is not known. Eight of the 10 Fzd genes were found to be expressed in F9 cells, with Fzd7 being the most highly expressed, and chosen for further analysis. To alter steady-state Fzd7 levels and test the effect this has on differentiation, siRNA and overexpression approaches were used to knock-down and ectopically express the Fzd7 message, respectively. siRNA knock-down of Fzd7 resulted in reduced DAB2 levels, and the overexpression activated a TCF–LEF reporter, but neither approach affected differentiation. Our focus turned to how canonical WNT6 signaling was attenuated to allow PrE cells to form parietal endoderm (PE). Dkk1, encoding a WNT antagonist, was examined and results showed that its expression increased in F9 cells treated with retinoic acid (RA) or overexpressing Wnt6. F9 cells overexpressing human DKK1 or treated with DKK1-conditioned medium and then treated with RA failed to differentiate, indicating that a negative feedback loop involving WNT6 and DKK1 attenuates canonical WNT–β-catenin signaling, thereby allowing PE cells to differentiate.

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.

Variant hepatocyte nuclear factor 1 is required for visceral endoderm specification

Development ◽  
1999 ◽  
Vol 126 (21) ◽  
pp. 4795-4805 ◽  
Author(s):  
E. Barbacci ◽  
M. Reber ◽  
M.O. Ott ◽  
C. Breillat ◽  
F. Huetz ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Embryonic Stem ◽  
Cell Lineage ◽  
Embryoid Bodies ◽  
Nuclear Factor ◽  
Visceral Endoderm ◽  
Hepatocyte Nuclear Factor ◽  
Parietal Endoderm ◽  
Nuclear Factor 1

Genetic and molecular evidence indicates that visceral endoderm, an extraembryonic cell lineage, is required for gastrulation, early anterior neural patterning, cell death and specification of posterior mesodermal cell fates. We show that variant Hepatocyte Nuclear Factor 1 (vHNF1), a homeodomain-containing transcription factor first expressed in the primitive endoderm, is required for the specification of visceral endoderm. vHnf1-deficient mouse embryos develop normally to the blastocyst stage, start implantation, but die soon afterwards, with abnormal or absent extraembryonic region, poorly organised ectoderm and no discernible visceral or parietal endoderm. However, immunostaining analysis of E5.5 nullizygous mutant embryos revealed the presence of parietal endoderm-like cells lying on an abnormal basal membrane. Homozygous mutant blastocyst outgrowths or differentiated embryonic stem cells do not express early or late visceral endoderm markers. In addition, in vHnf1 null embryoid bodies there is no activation of the transcription factors HNF-4alpha1, HNF1alpha and HNF-3gamma. Aggregation of vHnf1-deficient embryonic stem cells with wild-type tetraploid embryos, which contribute exclusively to extraembryonic tissues, rescues periimplantation lethality and allows development to progress to early organogenesis. Our results place vHNF1 in a preeminent position in the regulatory network that specifies the visceral endoderm and highlight the importance of this cell lineage for proper growth and differentiation of primitive ectoderm in pregastrulating embryos.

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