cytidylyl-3--5--guanosine has been researched along with Cell-Transformation--Neoplastic* in 2 studies
2 other study(ies) available for cytidylyl-3--5--guanosine and Cell-Transformation--Neoplastic
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De novo methylation of the MyoD1 CpG island during the establishment of immortal cell lines.
CpG dinucleotides are unevenly distributed in the vertebrate genome. Bulk DNA is depleted of CpGs and most of the cytosines in the dinucleotide in this fraction are methylated. On the other hand, CpG islands, which are often associated with genes, are unmethylated at testable sites in all normal tissues with the exception of genes on the inactive X chromosome. We used Hpa II/Msp I analysis and ligation-mediated polymerase chain reaction to examine the methylation of the MyoD1 CpG island in adult mouse tissues, early cultures of mouse embryo cells, and immortal fibroblastic cell lines. The island was almost devoid of methylation at CCGG sites in adult mouse tissues and in low-passage mouse embryo fibroblasts. In marked contrast, the island was methylated in 10T 1/2 cells and in six other immortal cell lines showing that methylation of this CpG island had occurred during escape from senescence. The island became even more methylated in chemically transformed derivatives of 10T 1/2 cells. Thus, CpG islands not methylated in normal tissues may become modified to an abnormally high degree during immortalization and transformation. Topics: Animals; Base Sequence; Blotting, Southern; Cell Line; Cell Transformation, Neoplastic; Clone Cells; Dinucleoside Phosphates; DNA; DNA Probes; Embryo, Mammalian; Methylation; Methylcholanthrene; Mice; Molecular Sequence Data; MyoD Protein; Nuclear Proteins; Oligonucleotide Probes; Phosphoproteins; Polymerase Chain Reaction; Restriction Mapping | 1990 |
Effect of CpG-rich sequences in transformation and tumorigenesis by polyomavirus.
To address the question of the role of CpG-rich sequences in gene expression, we investigated the effect of an HTF island on the activity of the polyomavirus middle T (pmt) oncogene. pmt is less transformant and less tumorigenic when it is introduced into cultured cells or newborn rats in the presence of an HTF island. Transformed cells carrying pmt in the vicinity of the HTF island have a propensity to revert at a relatively high rate of about 2 X 10(-3) per cell per generation by a mechanism probably involving methylation of some CpG sites in the island. Our results suggest that HTF islands can function as transcriptional silencers. Topics: Animals; Animals, Newborn; Antigens, Polyomavirus Transforming; Base Sequence; Blotting, Southern; Cell Line; Cell Transformation, Neoplastic; Dinucleoside Phosphates; DNA, Viral; Oncogenes; Plasmids; Polyomavirus; Rats; Transcription, Genetic | 1989 |