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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
Mol Cell Biol 1989 Aug
PMID:Control of beta-interferon expression in murine embryonal carcinoma F9 cells. 279 97

Retrovirus expression is restricted in embryonal carcinoma (EC) cells but not in many differentiated cell lines. We used a very sensitive gel retardation assay to detect sequence-specific DNA-binding proteins in crude nuclear extracts obtained from EC and differentiated cells. Four binding sites were mapped in the noncoding sequences of the amphotropic murine leukemia virus. Strong binding to the CCAAT consensus sequence located in the promoter was specifically observed with EC nuclear extract. The binding protein is called EPBF (embryonal promoter-binding factor), and it is a candidate for the repressor of retrovirus transcription.
Mol Cell Biol 1987 Oct
PMID:An embryonic DNA-binding protein specific for the promoter of the retrovirus long terminal repeat. 282 91

Polyomavirus (Py) enhancer core elements were compared for their ability to activate Py early transcription and DNA replication in mouse 3T6 cells, lymphoid cell lines, and undifferentiated embryonal carcinoma cells. By examining the pattern of genetic change in a number of cell-specific Py variants, we identified subenhancer sequences that may be functionally important for virus replication. Four such distinct enhancer consensus sequences were synthesized and designated as the A core (homologous with adenovirus 5 E1A enhancer), B core (homologous to the simian virus 40 A enhancer core), C core (containing an inverted repeat within the Py B enhancer), and BPV core (homologous to the bovine papillomavirus enhancer). When used to replace the complete Py B enhancer, single copies of all but the BPV element were able to fully activate Py DNA replication after transfection, but this activation was usually cell type specific. In the PCC4 embryonal carcinoma cells, only the A-core sequence was able to activate transcription and DNA replication. The BPV core sequence containing the Py F441 point change was unable to activate DNA replication in the F9 embryonal carcinoma or any other cell line. No single insertion element was dominant nor did these elements display the wild-type enhancer pattern of cell-specific activation of DNA replication. In addition, differential effects were often observed on the activation of transcription versus DNA replication. In 3T6 cells, transcription could be highly activated by the A core without a corresponding activation of DNA replication. In murine T lymphoid cell lines, the B core activated DNA replication without a corresponding increase in transcription. Furthermore, both DNA replication and, to a lesser degree, transcription often showed a strong tissue-specific dependence on the polarity of the inserted core element for activation.
Mol Cell Biol 1988 May
PMID:Functional analysis of the individual enhancer core sequences of polyomavirus: cell-specific uncoupling of DNA replication from transcription. 283 39

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.
Mol Cell Biol 1988 May
PMID:Establishment of composite DNA derived from L factor as a plasmid in mouse embryonal carcinoma (F9) cells. 283 42

The presence of the adenovirus E1A-like activity in embryonal carcinoma stem cells has been reported. We now show that preimplantation stage mouse embryonic cells allow transcription of the E1A-dependent E2A gene when infected with E1A-deleted mutant dl312, indicating the presence of the E1A-like activity in morulae and blastocysts. Moreover, such activity seems to decrease or disappear at about the time of implantation.
Mol Cell Biol 1988 Aug
PMID:Presence of the adenovirus E1A-like activity in preimplantation stage mouse embryos. 297 25

Circular, double-stranded DNA molecules were injected into nuclei of mouse oocytes and one- or two-cell embryos to determine whether specific sequences were required to replicate DNA during mouse development. Although all of the injected DNAs were stable, replication of plasmid pML-1 DNA was not detected unless it contained either polyomavirus (PyV) or simian virus 40 (SV40) DNA sequences. Replication occurred in embryos, but not in oocytes. PyV DNA, either alone or recombined with pML-1, underwent multiple rounds of replication to produce superhelical and relaxed circular monomers after injection into one- or two-cell embryos. SV40 DNA also replicated, but only 3% as well as PyV DNA. Coinjection of PyV DNA with either pML-1 or SV40 had no effect on the replicating properties of the three DNAs. These results are consistent with a requirement for specific cis-acting sequences to replicate DNA in mammalian embryos, in contrast to sequence-independent replication of DNA injected into Xenopus eggs. Furthermore, PyV DNA replication in mouse embryos required PyV large T-antigen and either the alpha-beta-core or beta-core configuration of the PyV origin of replication. Although the alpha-core configuration replicated in differentiated mouse cells, it failed to replicate in mouse embryos, demonstrating cell-specific activation of an origin of replication. Replication or expression of PyV DNA interfered with normal embryonic development. These results reveal that mouse embryos are permissive for PyV DNA replication, in contrast to the absence of PyV DNA replication and gene expression in mouse embryonal carcinoma cells.
Mol Cell Biol 1985 Nov
PMID:Sequence-dependent DNA replication in preimplantation mouse embryos. 301 87

We have identified a factor present in nuclear extracts of undifferentiated F9 murine embryonal carcinoma cells that specifically interacts with the polyomavirus enhancer region. Nuclease "footprint" analysis was used to define the binding site that corresponds precisely to the boundaries of polyoma enhancer element C defined by Veldman et al. [Veldman, G. M., Lupton, S. & Kamen, R. (1985) Mol. Cell. Biol. 5, 649-658] that is required as an enhancer for efficient viral DNA replication and early and late region transcription. The region of nuclease protection contains a 6-base-pair inverted repeat, separated by 3 base pairs, and symmetrical flanking DNase I hypersensitive cleavage sites, suggesting that this factor may bind as a dimer. A cloned 29-base-pair polyoma DNA fragment contains an intact binding domain. Similar levels of binding activity were found in nuclear extracts prepared from differentiated murine F9 cells, as well as murine L cells and human HeLa cells. The factor has been termed "EF-C" for enhancer binding factor to polyoma element C.
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PMID:Interaction of a nuclear factor with the polyomavirus enhancer region. 302 96

A derivative of the myeloproliferative sarcoma virus (Neor-MPSV) carrying the mos oncogene and dominant selection marker for neomycin resistance (Neor) was introduced into embryonal carcinoma and embryo-derived cell lines by transfection and infection using pseudotypes with Friend helper virus (Friend murine leukemia virus [F-MuLV]). Cells resistant to G418 (a neomycin analog) were cloned and expanded. Transductants retained an undifferentiated phenotype as judged by morphology, tumorigenicity, and cell-surface antigen analyses. Nucleic acid analysis of infectants revealed both Neor-MPSV and F-MuLV proviruses, although no virus was released. G418-resistant transductants remained nonpermissive for the expression of other proviruses and for subsequent superinfection. Northern analysis showed expression of full-length Neor-MPSV, as well as mos-specific subgenomic RNA. mos sequences were deleted from Neor-MPSV (Neor mos-1), and pseudotypes were used to infect embryonal carcinoma cells. No morphological differences were observed in either mos+ or mos- transductants as compared with parental cell lines. However, mos+ transductants showed an enhanced anchorage-independent growth compared with that of mos- transductants in agar cloning. PCC4 transductants were induced to differentiate with retinoic acid and superinfected with F-MuLV. Infection with viral supernatant in fibroblasts and in mice confirmed the rescue of biologically active Neor-MPSV.
Mol Cell Biol 1986 Jan
PMID:Viral transfer, transcription, and rescue of a selectable myeloproliferative sarcoma virus in embryonal cell lines: expression of the mos oncogene. 302 29

Heterologous enhancer recombinants and deletions of the polyomavirus (Py) noncoding region were constructed and analyzed for tissue specificity of DNA replication and transcription in a number of lymphoid and other cell lines. The simian virus 40 72-base-pair repeat, mouse immunoglobulin heavy-chain enhancer, and Moloney murine leukemia virus enhancer were inserted into the PvuII-D locus (nucleotides 5128 through 5265) of Py. The ability of these recombinants and the parental PvuII-D deletion mutant to replicate in permissive 3T6 cells and MOP-6 cells as well as in nonpermissive mouse B lymphoid, T lymphoid, mastocyte, and embryonal carcinoma cells was determined. Wild-type Py DNA was not permissive for replication in most lymphoid cell lines, except one hybridoma line. Simply deleting the Py PvuII-D region, however, gave Py an expanded host range, allowing high-level replication in some T lymphoid and mastocytoma cell lines, indicating that this element can be a tissue-specific negative as well as positive element. Substitution of the murine leukemia virus enhancer for Py PvuII-D yielded a Py genome which retained the ability to replicate in 3T6 cells but also replicated well in B lymphoid cells. Substitution with the immunoglobulin heavy-chain enhancer allowed replication in B lymphoid cells but interfered with replication in 3T6 cells and mastocytomas. Surprisingly, substitution with the simian virus 40 72-base-pair enhancer repeat gave a recombinant which would not replicate in any cell line tried, including MOP-6 cells, even though other recombinants with this enhancer would replicate. Thus, we observed both cooperation and interference in these combinations between enhancer components and the Py genome and that these combined activities were cell specific. These results are presented as evidence that there may be a positional dependence, or syntax, for the recognition of genetic elements controlling Py tissue specificity.
Mol Cell Biol 1986 Jun
PMID:Lymphoid and other tissue-specific phenotypes of polyomavirus enhancer recombinants: positive and negative combinational effects on enhancer specificity and activity. 302 17

A small circular DNA was found extrachromosomally in a clone of F9 embryonal carcinoma (EC) cells at high copy numbers per cell. The DNA was cloned in plasmid pUC19. Restriction endonuclease analyses of the DNA indicated that the DNA (fPyF9) was a mutant of polyomavirus (Py) DNA and had a mutation in a noncoding regulatory region. There have been many reports on the isolation of Py mutants capable of replication in undifferentiated cells. However, fPyF9 was different from other Py mutants in the following aspects: it was harbored stably as a free copy at 1 X 10(4) to 5 X 10(4) copies per cell in EC cells; it replicated in undifferentiated cells better than in differentiated cells; it was extremely rearranged in the sequences of the enhancer B domain; and it carried in the enhancer B domain three copies of an exogenous sequence which does not exist in Py strain A2. From these observations, we propose a new class of Py EC mutant which has an autonomous state similar to that of plasmid and small circular DNA in host cells.
Mol Cell Biol 1986 Nov
PMID:New class of polyomavirus mutant that can persist as free copies in F9 embryonal carcinoma cells. 302 19


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