Cyclic amp-induced morphological transformation of cells infected by temperature-sensitive mouse sarcoma virus: Expression of transformation-associated markers

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Abstract
Normal rat kidney (NRK) cells infected with a temperature-sensitive (ts) mutant of mouse sarcoma virus (NRK[MSV-1b]) express the transformed phenotype under permissive conditions, but acquire the normal phenotype when grown under restrictive conditions. Addition of cyclic[c]AMP to NRK(MSV-1b) cells grown at the restrictive temperature results in morphological transformation. To determine whether other markers associated with the transformed phenotype were coordinately expressed after cAMP exposure, concanavalin A (Con A) agglutinability, hexose transport rate and incorporation of radioactively labeled fucose into fucolipid III and fucolipid IV (FL III and FL IV) of the cells were examined. NRK cells transformed by wild-type MSV or NRK(MSV-1b) grown under permissive conditions were agglutinated by low concentrations of Con A and exhibited relatively high maximal agglutination levels which were specifically inhibited by .alpha.-methyl-D-mannoside. NRK(MSV-1b) cells grown under restrictive conditions were weakly agglutinated by Con A and exhibited reduced maximal agglutination levels, similar to uninfected NRK cells. Treatment of NRK(MSV-1b) cells at the restrictive temperature with cAMP resulted in morphological transformation and a change in the pattern of incorporation of labeled fucose into FL III and FL IV to one comparable to that of NRK(MSV-1b) cells at the permissive temperature or NRK cells transformed by wild-type MSV. cAMP treatment resulted in no increase in Con A agglutinability or 2-deoxy-D-[3H]glucose transport relative to mock treated cultures. cAMP-induced morphological transformation and altered fucolipid composition of NRK(MSV-1b) cells are not correlated with alterations in hexose transport rate or Con A agglutinability.
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