Straaten H, Weber K J, Kiefer J
Strahlenzentrum der Justus-Liebig-Universität Giessen, Germany.
Radiat Res. 1992 Feb;129(2):177-83.
Excision-deficient haploid yeast cells (Saccharomyces cerevisiae) were exposed to 254-nm UV radiation and protein synthesis inhibition was measured for a large number of different proteins resolved by two-dimensional gel electrophoresis. The derived UV-radiation sensitivities exhibited an overall increase with protein molar mass. Quantitatively, this behavior is compatible with a well known mechanism of transcription inactivation--termination of RNA chains at UV-radiation-induced pyrimidine dimers--if the respective target sizes are inferred from protein molar mass. The observed deviations from the predicted response suggest that (i) UV-radiation damage may also interfere with recognition/binding of RNA polymerase to regulatory sequences and (ii) the frequency of photolesions for a specific protein encoding gene may differ markedly from the mean induction rate for the total yeast genome.
将切除缺陷型单倍体酵母细胞（酿酒酵母）暴露于254纳米的紫外线辐射下，并通过二维凝胶电泳对大量不同蛋白质进行蛋白质合成抑制测定。得出的紫外线辐射敏感性总体上随蛋白质摩尔质量增加而升高。从定量角度来看，如果从蛋白质摩尔质量推断出各自的靶标大小，这种行为与一种众所周知的转录失活机制——紫外线辐射诱导的嘧啶二聚体处RNA链的终止——是相符的。观察到的与预测反应的偏差表明：（i）紫外线辐射损伤也可能干扰RNA聚合酶与调控序列的识别/结合；（ii）特定蛋白质编码基因的光损伤频率可能与整个酵母基因组的平均诱导率显著不同。
