Relationship between chromosome condensation and metaphase lysine-rich histone phosphorylation.

Abstract

Treatment of metaphase rat hepatoma HTC cells with ZnCl2 inhibits histone phosphatase activity and leads to an increase in the hyperphosphorylated forms of the lysine-rich (F1) histone. Under normal conditions a massive phosphatase activity is triggered as the cells shift from M into G1 phase. In the presence of ZnCl2 this activity is abolished and the hyperphosphorylated form of F1 persists intact into G1. An apparently normal extension of chromosome material occurs during the M-G1 transition even if the F1 histone is maintained in the hyperphosphorylated form. High levels of ZnCl2 have rather substantial effects on other cell functions.