scholarly journals JDP2, a Repressor of AP-1, Recruits a Histone Deacetylase 3 Complex To Inhibit the Retinoic Acid-Induced Differentiation of F9 Cells

2002 ◽  
Vol 22 (13) ◽  
pp. 4815-4826 ◽  
Author(s):  
Chunyuan Jin ◽  
Hongjie Li ◽  
Takehide Murata ◽  
Kailai Sun ◽  
Masami Horikoshi ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Histone Deacetylase ◽  
Chromatin Immunoprecipitation ◽  
Embryonal Carcinoma ◽  
Critical Event ◽  
F9 Cells ◽  
Histone Deacetylase 3 ◽  
Activation Of Transcription ◽  
Key Factor ◽  
Activating Transcription Factor

ABSTRACT Up-regulation of the c-jun gene is a critical event in the retinoic acid (RA)-mediated differentiation of embryonal carcinoma F9 cells. Activating transcription factor 2 (ATF-2) and p300 cooperate in the activation of transcription of the c-jun gene during the differentiation of F9 cells. We show here that the overexpression of Jun dimerization protein 2 (JDP2), a repressor of AP-1, inhibits the transactivation of the c-jun gene by ATF-2 and p300 by recruitment of the histone deacetylase 3 (HDAC3) complex, thereby repressing the RA-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Moreover, chromatin immunoprecipitation assays showed that the JDP2/HDAC3 complex, which binds to the differentiation response element within the c-jun promoter in undifferentiated F9 cells, was replaced by the p300 complex in response to RA, with an accompanying change in the histone acetylation status of the chromatin, the initiation of transcription of the c-jun gene, and the subsequent differentiation of F9 cells. These results suggest that JDP2 may be a key factor that controls the commitment of F9 cells to differentiation and shed new light on the mechanism by which an AP-1 repressor functions.

Control of beta-interferon expression in murine embryonal carcinoma F9 cells

1989 ◽  
Vol 9 (8) ◽  
pp. 3553-3556
Author(s):  
M K Francis ◽  
J M Lehman
Keyword(s):  
Retinoic Acid ◽  
Embryonal Carcinoma ◽  
Biologically Active ◽  
Rnase Protection ◽  
F9 Cells ◽  
Differentiated Cells ◽  
Transcriptional Regulatory Mechanism ◽  
Transcriptional Regulatory ◽  
Tissue Culture Model

Murine embryonal carcinoma F9 cells, a tissue culture model for early embryonic development, do not produce interferon (IFN) in response to poly(I-C), as determined by an antiviral assay. RNase protection analyses were used to examine total RNA extracted from the cells for the presence of beta-IFN RNA. Whereas F9 cells differentiated in vitro with retinoic acid produced a biologically active protein as well as beta-IFN RNA in response to poly(I-C), undifferentiated F9 cells produced no detectable beta-IFN RNA even in the presence of cycloheximide, an IFN-superinducing agent. These results show that undifferentiated embryonal carcinoma cells do not accumulate beta-IFN RNA in response to an IFN-inducing agent, suggesting a transcriptional regulatory mechanism. However, this control mechanism is altered upon differentiation, since the gene can be transcriptionally activated in retinoic acid-differentiated cells.

scholarly journals Establishment of composite DNA derived from L factor as a plasmid in mouse embryonal carcinoma (F9) cells.

1988 ◽  
Vol 8 (5) ◽  
pp. 2097-2104 ◽  
Author(s):  
K Nishimori ◽  
T Kohda ◽  
J Fujiwara ◽  
M Oishi
Keyword(s):  
Gene Expression ◽  
Escherichia Coli ◽  
Retinoic Acid ◽  
Plasmid Dna ◽  
Inverse Relationship ◽  
Embryonal Carcinoma ◽  
Foreign Gene ◽  
In Vitro Differentiation ◽  
F9 Cells

We have recently reported a mammalian cell plasmid (L factor) whose structure is related to that of polyomavirus (T. Kusano, H. Uehara, H. Saito, K. Segawa, and M. Oishi, Proc. Natl. Acad. Sci. USA 84:1789-1793, 1987). When composite DNA constructed from L factor and a foreign gene was introduced into mouse embryonal carcinoma (F9) cells by transfection, the DNA was reestablished in the cells as a plasmid. The reestablished plasmid DNA in F9 cells could be rescued in Escherichia coli. The plasmid-bearing cells underwent normal in vitro differentiation in response to retinoic acid. The efficiency of plasmid establishment of the L-factor-derived DNA and transcriptional and transient replicational activities were compared with those of similar composite DNA constructed from polyomavirus and an embryonal carcinoma mutant of polyomavirus which is permissive in F9 cells. The results suggest an inverse relationship between the efficiency of the plasmid establishment and the activity of gene expression controlled by the intrinsic enhancer-promoter of the DNA.

Expression of the intracisternal A-particle is elevated during differentiation of embryonal carcinoma cells

1986 ◽  
Vol 6 (1) ◽  
pp. 150-157 ◽  
Author(s):  
C C Howe ◽  
G C Overton
Keyword(s):  
Retinoic Acid ◽  
Embryonal Carcinoma ◽  
Cell Types ◽  
Endogenous Retrovirus ◽  
Cdna Clones ◽  
Embryonal Carcinoma Cell ◽  
Proviral Sequence ◽  
F9 Cells ◽  
Embryonal Carcinoma Cell Line ◽  
Intracisternal A Particle

Three cDNA clones coding for the 3' region of the intracisternal A-particle (IAP), a mouse endogenous retrovirus, were isolated during screening of a library for genes whose expression was modulated during the retinoic acid-induced differentiation of the embryonal carcinoma cell line F9 into parietal endoderm-like (PE-like) cells. In contrast to previously reported results, no IAP transcripts were detected in either F9 cells or two pluripotent cell lines tested. Instead, IAP transcripts as well as IAPs were abundant in the PE-like cells PYS-2 and F9AcCl 9 and in retinoic acid-induced F9 cells but not in the other differentiated cell types of teratocarcinoma origin which were examined. A comparison of the nucleotide sequences of the three IAP cDNA clones with a genomically integrated proviral sequence (MIA14) demonstrated heterogeneity in both length and sequence among the clones. The position of the poly(A) addition site was determined to be 15 nucleotides from the proposed poly(A) addition signal and to occur after the sequence CAGA, not CA, as previously proposed. Length heterogeneity was greatest in a region of TC repeats 80 base pairs 5' to the poly(A) addition site. Additionally, the putative TATAA box found in MIA14 was deleted in the cDNA clones and in the long terminal repeat regions from two other genomic clones examined. The heterogeneity evident among the cDNA clones further demonstrated that at least two distinct IAP genes are activated during differentiation. An analysis of the rate of transcription in isolated nuclei indicated that the activation of expression of IAP genes in PE-like cells is the result of transcriptional regulation. Together, these observations suggest that the modulation of IAP transcription is regulated autonomously rather than by the fortuitous integration of an IAP sequence adjacent to a developmentally regulated cellular gene.

Expression of Oct-4 during differentiation of murine F9 cells

1996 ◽  
Vol 74 (4) ◽  
pp. 579-584 ◽  
Author(s):  
Liangsu Wang ◽  
Gilbert A. Schultz
Keyword(s):  
Transcription Factor ◽  
Retinoic Acid ◽  
Embryonal Carcinoma ◽  
Embryonic Stem ◽  
Carcinoma Cells ◽  
Peptide Sequence ◽  
Structural Motif ◽  
Embryonal Carcinoma Cells ◽  
Western Blots ◽  
F9 Cells

Oct-4 is a transcription factor that shares a common structural motif with members of the POU family. The mRNA for Oct-4 is found in growing oocytes and in totipotent or pluripotent cells of the early mouse embryo. Oct-4 is down-regulated in embryos during differentiation events associated with blastocyst implantation and gastrulation. Oct-4 gene expression is also down-regulated when murine embryonic stem cells or embryonal carcinoma cells are induced to differentiate in the presence of retinoic acid. A polyclonal antibody that can recognize a unique peptide sequence in the C-terminus of mouse Oct-4 has been prepared. It specifically recognizes Oct-4 protein as tested by Western blots and gel mobility shift assays. This antibody has been used to measure Oct-4 protein levels during retinoic acid induced differentiation of F9 embryonal carcinoma cells. It was observed that Oct-4 protein was abundant in undifferentiated F9 cells but decreased to levels below detection as the cells differentiated, consistent with changes in levels of expression in early embryos.Key words: octamer, DNA-binding protein, transcription factor, embryonal carcinoma cells.

scholarly journals Expression of the intracisternal A-particle is elevated during differentiation of embryonal carcinoma cells.

1986 ◽  
Vol 6 (1) ◽  
pp. 150-157 ◽  
Author(s):  
C C Howe ◽  
G C Overton
Keyword(s):  
Retinoic Acid ◽  
Embryonal Carcinoma ◽  
Cell Types ◽  
Endogenous Retrovirus ◽  
Cdna Clones ◽  
Embryonal Carcinoma Cell ◽  
Proviral Sequence ◽  
F9 Cells ◽  
Embryonal Carcinoma Cell Line ◽  
Intracisternal A Particle

Three cDNA clones coding for the 3' region of the intracisternal A-particle (IAP), a mouse endogenous retrovirus, were isolated during screening of a library for genes whose expression was modulated during the retinoic acid-induced differentiation of the embryonal carcinoma cell line F9 into parietal endoderm-like (PE-like) cells. In contrast to previously reported results, no IAP transcripts were detected in either F9 cells or two pluripotent cell lines tested. Instead, IAP transcripts as well as IAPs were abundant in the PE-like cells PYS-2 and F9AcCl 9 and in retinoic acid-induced F9 cells but not in the other differentiated cell types of teratocarcinoma origin which were examined. A comparison of the nucleotide sequences of the three IAP cDNA clones with a genomically integrated proviral sequence (MIA14) demonstrated heterogeneity in both length and sequence among the clones. The position of the poly(A) addition site was determined to be 15 nucleotides from the proposed poly(A) addition signal and to occur after the sequence CAGA, not CA, as previously proposed. Length heterogeneity was greatest in a region of TC repeats 80 base pairs 5' to the poly(A) addition site. Additionally, the putative TATAA box found in MIA14 was deleted in the cDNA clones and in the long terminal repeat regions from two other genomic clones examined. The heterogeneity evident among the cDNA clones further demonstrated that at least two distinct IAP genes are activated during differentiation. An analysis of the rate of transcription in isolated nuclei indicated that the activation of expression of IAP genes in PE-like cells is the result of transcriptional regulation. Together, these observations suggest that the modulation of IAP transcription is regulated autonomously rather than by the fortuitous integration of an IAP sequence adjacent to a developmentally regulated cellular gene.

Retinoic acid induces activin receptor IIB mRNA in F9 embryonal carcinoma cells

1995 ◽  
Vol 14 (2) ◽  
pp. 247-254 ◽  
Author(s):  
Y-J Y Wan ◽  
L Wang ◽  
T-C J Wu
Keyword(s):  
Gene Expression ◽  
Retinoic Acid ◽  
Embryonal Carcinoma ◽  
Actinomycin D ◽  
Inductive Effect ◽  
Receptor Type ◽  
Dependent Manner ◽  
Mrna Isoforms ◽  
Activin Receptor ◽  
F9 Cells

ABSTRACT Mouse embryonal carcinoma F9 cells are pluripotent stem cells and differentiate into primitive endodermal cells upon treatment with retinoic acid (RA). We have recently shown that in F9 cells RA regulates gene expression of activin receptor type II (ActR-II), whose ligand is a potent differentiation agent. The present study examined the regulation of the newly cloned activin receptor type IIB (ActR-IIB) gene by RA. F9 cells expressed equal amounts of three ActR-IIB transcripts of 8·0, 7·5 and 4·0 kb. Both 9-cis-RA (c-RA) and all-trans-RA (t-RA) induced ActR-IIB gene expression in a dose-dependent manner. At 10−9m c-RA exerted no effect, while 10−5m c-RA increased the 8·0 kb ActR-IIB transcript about sevenfold. In contrast, t-RA induced the 8·0kb ActR-IIB transcript fivefold at 10−9m and up to eightfold at 10−5m. The inductive effect on the 8·0 kb transcript was greater than that on the 7·5 kb transcript, and was least effective on the 4·0 kb transcript, suggesting that these three mRNA isoforms may originate from different promoters. Both cycloheximide and actinomycin D inhibited the inductive effect of t-RA on ActR-IIB gene expression, in contrast to ActR-II whose gene expression was not suppressed by cycloheximide but abolished by actinomycin D. Thus, endodermal differentiation of F9 cells is associated with activation of ActR-IIB gene and the mechanisms involved in the regulation of ActR-II and IIB gene expression are different.

Sign in / Sign up

Export Citation Format

Share Document