Tunicamycin inhibits the initiation of DNA synthesis stimulated by prostaglandin F2αin Swiss mouse 3T3 cells

Tunicamycin, an inhibitor of the asparagine‐linked protein N‐glycosylation, blocks the initiation of DNA synthesis in Swiss 3T3 cells stimulated by prostaglandin F2αalone or with insulin. This effect is exerted only when tunicamycin is added from 0 to 8 h after stimulation and it decreases the rate of entry into S phase. Blocking of labeled sugar incorporation to proteins occurs regardless of the time of PGF2αstimulation. In contrast tunicamicin does not inhibit protein synthesis. These results suggest that N‐glycoprotein synthesis early during the prereplicative phase is an important event controlling the mitogenic action of PGF2α