Ajiro K, Nishimoto T, Takahashi T
J Biol Chem. 1983 Apr 10;258(7):4534-8.
The histone phosphorylations of temperature-sensitive mutant cells (tsBN2) were investigated during the induction of premature chromosome condensation (PCC). At the permissive temperature (33.5 degrees C), the histones of the cells were phosphorylated typically as in any other mammalian cell. However, at the nonpermissive temperature (40.5 degrees C), both histone H1 and H3 were phosphorylated extensively as in mitotic cells, and the increase in these phosphorylations throughout S to G2 phase was closely correlated to the frequency of cells showing PCC. The pattern of H1 subtype phosphorylations was quite similar, and the sites of H1 phosphorylation from PCC were the same as those from mitotic cells. Although the degree of phosphorylation was low, H1 and H3 phosphorylations were observed even in G1 phase at the nonpermissive temperature. The effects of metabolic inhibitors on the induction of PCC were parallel in H1 and H3 phosphorylations; actinomycin D failed to inhibit either PCC induction or these phosphorylations, whereas cyclohexamide did, completely inhibiting H3 phosphorylation.
在早熟染色体凝聚（PCC）诱导过程中，对温度敏感突变细胞（tsBN2）的组蛋白磷酸化进行了研究。在允许温度（33.5摄氏度）下，这些细胞的组蛋白磷酸化情况与其他任何哺乳动物细胞一样典型。然而，在非允许温度（40.5摄氏度）下，组蛋白H1和H3都像在有丝分裂细胞中一样大量磷酸化，并且在整个S期到G2期这些磷酸化的增加与显示PCC的细胞频率密切相关。H1亚型磷酸化模式非常相似，来自PCC的H1磷酸化位点与来自有丝分裂细胞的相同。尽管磷酸化程度较低，但在非允许温度下，即使在G1期也观察到了H1和H3的磷酸化。代谢抑制剂对PCC诱导的影响在H1和H3磷酸化方面是平行的；放线菌素D未能抑制PCC诱导或这些磷酸化，而环己酰亚胺则可以，它完全抑制了H3磷酸化。
