Abstract
Morphological transformation of normal mouse embryo cells by murine sarcoma virus (MOLONEY) and subsequent development of murine sarcoma virus growth were investigated using cytosine arabinoside (ara-C) and X-irradiation. Inhibition of DNA synthesis, cell division and transformation by ara-C were all reversible by deoxycytidine. The susceptibility of mouse embryo cells to infection and morphological transformation was most sensitive to ara-C during the first 6 hr after the virus-cell encounter. Sensitivity decreased with time, and by 24 to 48 hr virtually all infected cells had become transformed and completed the virus growth cycle, despite ara-C treatment. Irradiation of transformed, virus-producing cells with either 5000 R or 100,000 R had little effect on the ability of infected cells to produce murine sarcoma virus 24 hr later, and about 10% irradiated cells were still producing virus after 48 hr. Radiation survival and heat (37°) inactivation data for murine sarcoma virus (MOLONEY) are presented. The results indicate that the successful infection and morphological transformation of normal mouse embryo cells by murine sarcoma virus (MOLONEY) requires a DNA synthetic event immediately after the virus-cell encounter and, that once initiated, successful virus growth no longer depends on DNA synthesis.