The adenovirus Ela gene induces differentiation of F9 teratocarcinoma cells.
Undifferentiated F9 cells transfected with plasmids encoding adenovirus E1a gene products underwent radical morphological changes. They ceased to express the SSEA-1 stem cell marker antigen and started to express a number of the characteristics of the differentiated state that is induced in F9 cells by treatment with retinoic acid. In particular, they expressed keratin intermediate filaments and acquired the ability to synthesise simian virus 40 tumor antigens after virus infection. The transfected cells expressed the E1a proteins, and this expression was necessary to induce the phenotypic changes, since a coisogenic plasmid encoding only a truncated 70-amino-acid E1a polypeptide and the transfection procedure itself did not detectably after the morphology or marker expression of the F9 stem cells. The phenotypic change was induced by both 13S and 12S cDNA plasmids. We discuss these results in the context of known E1a functions and with reference to the other oncogenes and external factors that can cause F9 cell differentiation.
D017456:Adenovirus Early Proteins; D000260:Adenoviruses, Human / Q000235:genetics*; D000954:Antigens, Surface / Q000032:analysis; D000957:Antigens, Viral, Tumor / Q000235:genetics; D002454:Cell Differentiation; D002455:Cell Division; D007633:Keratins / Q000096:biosynthesis; D009856:Oncogene Proteins, Viral / Q000502:physiology*; D013539:Simian virus 40 / Q000235:genetics; D013724:Teratoma / Q000473:pathology; D014162:Transfection
D017456:Adenovirus Early Proteins; D000954:Antigens, Surface; D000957:Antigens, Viral, Tumor; D009856:Oncogene Proteins, Viral; D007633:Keratins