AbstractAt 37°C, undifferentiated murine teratocarcinoma cells (PCC4) are resistant to infection with SV40 and Polyoma virus. When infection is carried out at 31°C, these cells become fully susceptible to a variety of polyoma virus strains, includingwt,ts‐a, andhr‐t; they also display an increased susceptibility to polyoma virus mutants (PyE.C.) which have been selected for their ability to develop in PCC4 cells at 37°C (Vasseur et al., '80). However, expression of SV40 is still restricted at 31°C and no T antigen can be detected. PCC4 cells grown at 31°C express the characteristic embryonal surface antigen(s), but no H2 antigen, and do not produce plasminogen activator.PyE.C. mutants and other polyoma virus strains cannot develop at 37°C in nullipotent F9 embryonal carcinoma cells and restriction is not abolished at 31°C.The results indicate that: (i) Resistance of PCC4 cells to polyoma virus and to SV40 are not mediated by the same process; (ii) loss of restriction of polyoma in PCC4 cells does not require cell differentiation; (iii) F9 and PCC4 cells control polyoma virus expression through different
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