Chabanas A, Khoury E, Goeltz P, Froussard P, Gjerset R, Dod B, Eisen H, Lawrence J J
J Mol Biol. 1985 May 25;183(2):141-51. doi: 10.1016/0022-2836(85)90208-6.
We have examined the regulation of the synthesis of histone H1(0) in cultured mammalian cells treated with butyric acid. Treatment of cells with the inducer results in the arrest of synthesis of DNA and the other histones, while increasing the synthesis of H1(0) by a factor of 11. The induction of H1(0) by butyric acid occurs in a pulse with a peak at six hours, followed by a decrease to negligible levels. This pulse-like induction appears to be due to the fact that the cells are inducible for H1(0) only in the late S or G2 phases of the cell cycle. This, coupled with the fact that butyric acid blocks cells in G1, results in the burst of H1(0) synthesis after addition of the inducer. The G1 block provoked by butyric acid does not appear to result from the accumulation of H1(0). Removal of butyric acid from G1-blocked cells resulted in the resumption of cellular proliferation without prior loss of H1(0), demonstrating that the presence of this histone is not sufficient to prevent cellular proliferation.
我们研究了用丁酸处理的培养哺乳动物细胞中组蛋白H1(0)合成的调控。用诱导剂处理细胞会导致DNA和其他组蛋白的合成停止，同时H1(0)的合成增加11倍。丁酸对H1(0)的诱导呈脉冲式，在6小时达到峰值，随后降至可忽略不计的水平。这种脉冲式诱导似乎是由于细胞仅在细胞周期的S期晚期或G2期可被诱导合成H1(0)。这一点，再加上丁酸使细胞阻滞在G1期，导致添加诱导剂后H1(0)合成的爆发。丁酸引起的G1期阻滞似乎不是由H1(0)的积累导致的。从G1期阻滞的细胞中去除丁酸会导致细胞增殖恢复，而H1(0)并未预先丢失，这表明这种组蛋白的存在不足以阻止细胞增殖。
