Abstract
Embryonal carcinoma cells are resistant to infection by polyomavirus (Py). We showed that this block was partially removed by inhibiting protein synthesis temporarily. The block was also partially removed when Py was coinfected with simian virus 40. Cycloheximide treatment of cells infected with Py mutants able to grow on PCC4 embryonal carcinoma cells led to 3- to 10-fold increases in the production of T-antigen-positive cells. At 31 degrees C, Py T-antigen expression was enhanced when the cells were treated with cycloheximide. We suggest that a negative labile regulatory protein(s) is synthesized in PCC4 cells, preventing the initiation of early Py transcription by binding to the noncoding sequence, especially the enhancer element B and perhaps also element A, and that the Py mutants retained a binding site(s).
MeSH Terms
Animals
Antigens, Viral, Tumor/genetics
Cell Line
Cycloheximide/pharmacology
Embryonal Carcinoma Stem Cells
Enhancer Elements, Genetic
Gene Expression Regulation
Genes, Viral
Mice
Neoplastic Stem Cells/metabolism,microbiology
Polyomavirus/genetics,immunology
Protein Biosynthesis
Simian virus 40/physiology
Transcription, Genetic
Chemicals
Antigens, Viral, Tumor
Cycloheximide
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Cremisi C
Babinet C
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