Premium
Temperature dependent expression of polyoma virus in murine embryonal carcinoma cells
Author(s) -
Dandolo L.,
Vasseur M.,
Kress C.,
Aghion J.,
Blangy D.
Publication year - 1980
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041050104
Subject(s) - teratocarcinoma , embryonal carcinoma , microbiology and biotechnology , virus , biology , polyoma virus , mutant , cell culture , antigen , activator (genetics) , virology , cellular differentiation , gene , biochemistry , immunology , genetics
At 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, including wt , ts ‐ a , and hr ‐ 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 mechanisms.