Bergqvist A, Magnusson G
Department of Medical Virology, Uppsala University, Sweden.
Exp Cell Res. 1994 Nov;215(1):223-7. doi: 10.1006/excr.1994.1335.
Okadaic at low concentrations specifically inhibits protein phosphatase 2A. Treatment of cells with this inhibitor leads to growth arrest and cell injury within 1 to 2 days. After testing several different types of cells we found that mouse 3T6 cells and insect Sf9 cells responded to okadaic acid by apoptosis, as defined by changes in morphology and degradation of chromatin to fragments of nucleosome size. Infection of insect cells by baculovirus prevented the okadaic acid-induced apoptosis. Analysis of phosphoprotein synthesis by polyacrylamide gel electrophoresis showed that okadaic acid treatment resulted in hyperphosphorylation of some cellular proteins, including histone H1. Concomitant baculovirus infection of the cells did not change the overall phosphorylation pattern, but appeared to mitigate the okadaic acid-induced hyperphosphorylation of histone H1.
