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Induction of cellular deoxyribonucleic acid synthesis in butyrate-treated cells by simian virus 40 deoxyribonucleic acid.

机译:猿猴病毒40脱氧核糖核酸在丁酸酯处理的细胞中诱导细胞脱氧核糖核酸的合成。

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摘要

Sodium butyrate (3 mM) inhibited the entry into the S phase of quiescent 3T3 cells stimulated by serum, but had no effect on the accumulation of cellular ribonucleic acid. Simian virus 40 infection or manual microinjection of cloned fragments from the simian virus 40 A gene caused quiescent 3T3 cells to enter the S phase even in the presence of butyrate. NGI cells, a line of 3T3 cells transformed by simian virus 40, grew vigorously in 3 mM butyrate. Homokaryons were formed between G1 and S-phase 3T3 cells, Butyrate inhibited the induction of deoxyribonucleic acid synthesis that usually occurs in B1 nuclei when G1 cells are fused with S-phase cells. However, when G1 3T3 cells were fused with exponentially growing NGI cells, the 3T3 nuclei were induced to enter deoxyribonucleic acid synthesis. In tsAF8 cells, a ribonucleic acid polymerase II mutant that stops in the G1 phase of the cell cycle, no temporal sequence was demonstrated between the butyrate block and the temperature-sensitive block. These results confirm previous reports that certain virally coded proteins can induce cell deoxyribonucleic acid synthesis in the absence of cellular functions that are required by serum-stimulated cells. Our interpretation of these data is that butyrate inhibited cell growth by inhibiting the expression of genes required for the G0 leads to G1 leads to S transition and that the product of the simian virus 40 A gene overrode this inhibition by providing all of the necessary functions for the entry into the S phase.
机译:丁酸钠(3 mM)抑制了血清刺激的静止3T3细胞进入S期,但对细胞核糖核酸的积累没有影响。猿猴病毒40感染或手动显微注射猿猴病毒40 A基因的克隆片段后,即使存在丁酸盐,静态3T3细胞也进入S期。 NGI细胞是由猿猴病毒40转化的3T3细胞系,在3 mM丁酸盐中生长旺盛。在G1和S期3T3细胞之间形成了同核体,丁酸抑制了G1细胞与S期细胞融合时通常在B1核中发生的脱氧核糖核酸合成的诱导。但是,当G1 3T3细胞与成倍增长的NGI细胞融合时,会诱导3T3核进入脱氧核糖核酸合成。在tsAF8细胞中,它是一个核糖核酸聚合酶II突变体,在细胞周期的G1期停止,在丁酸酯嵌段和温度敏感嵌段之间未显示时间顺序。这些结果证实了以前的报道,即某些病毒编码蛋白可以在缺乏血清刺激的细胞所需的细胞功能的情况下诱导细胞脱氧核糖核酸的合成。我们对这些数据的解释是,丁酸酯通过抑制G0所需基因的表达来抑制细胞生长,从而导致G1导致S过渡,而猿猴病毒40 A基因的产物通过提供所有必需的功能来克服这种抑制作用。进入S阶段。

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