Bynum J W, Volkin E
J Cell Physiol. 1976 Jun;88(2):197-206. doi: 10.1002/jcp.1040880209.
When human myeloma cells are pulsed for one hour with 3H-uridine and chased for six hours in fresh medium containing unlabeled uridine, the processing of 45 S rRNA precursor into the stable 28 S and 18 S rRNA components can be followed. However, when the cells are chased in exogenous adenosine instead of uridine, the accumulation of 18 S rRNA is selectively inhibited. Cells pulsed with 3H-adenosine and chased in the absence of exogenous nucleosides exhibit normal rRNA precursor processing, while cells pulsed simultaneously with 3H-uridine and 3H-adenosine and chased with uridine and adenosine are deficient in labeled 18 S rRNA. Consequently, the inhibition of 18 S rRNA accumulation by adenosine is not an artifact of labeling nor is it relieved by an equal molar concentration of uridine. The wasting of 18 S rRNA in human myeloma cells is similar to that reported to occur in normal lymphocytes during the quiescent state.
当用人骨髓瘤细胞与³H - 尿苷脉冲处理1小时,并在含有未标记尿苷的新鲜培养基中追踪6小时时,可追踪45S rRNA前体加工成稳定的28S和18S rRNA组分的过程。然而,当细胞用外源性腺苷而非尿苷进行追踪时,18S rRNA的积累会被选择性抑制。用³H - 腺苷脉冲处理并在无外源性核苷的情况下追踪的细胞表现出正常的rRNA前体加工过程,而同时用³H - 尿苷和³H - 腺苷脉冲处理并用尿苷和腺苷追踪的细胞中,标记的18S rRNA缺乏。因此,腺苷对18S rRNA积累的抑制既不是标记的假象,也不会被等摩尔浓度的尿苷缓解。人骨髓瘤细胞中18S rRNA的损耗与据报道在静止状态下正常淋巴细胞中发生的情况相似。