Reed S I, Stark G R, Alwine J C
Proc Natl Acad Sci U S A. 1976 Sep;73(9):3083-7. doi: 10.1073/pnas.73.9.3083.
During lytic infection by simian virus 40, gene A is transcribed into early RNA, which is translated into A protein (T antigen). Both the rate of synthesis and the intracellular amount of early RNA are higher in cells infected by temperature-sensitive A (tsA) mutants than in cells infected by wild-type virus. These differences are observed at permissive temperature (32 degrees) and are amplified greatly after a shift to restrictive temperature (41 degrees). For example, at 32 degrees cells infected by tsA mutants synthesize early RNA approximately twice as fast as cells infected by wild-type virus. After the shift to 41 degrees, the rate of synthesis in the tsA infection increases to 15 times the rate in the wild-type infection. In contrast, cells infected by tsA mutants do not overproduce late RNA. We suggest that the A protein regulates its own synthesis by negative feedback control of gene A transcription.
在猴病毒40进行裂解感染期间，基因A被转录成早期RNA，后者被翻译成A蛋白（T抗原）。在受温度敏感型A（tsA）突变体感染的细胞中，早期RNA的合成速率和细胞内含量均高于受野生型病毒感染的细胞。这些差异在允许温度（32摄氏度）下即可观察到，并且在转移至限制温度（41摄氏度）后会大幅放大。例如，在32摄氏度时，受tsA突变体感染的细胞合成早期RNA的速度约为受野生型病毒感染细胞的两倍。转移至41摄氏度后，tsA感染中的合成速率增加至野生型感染中速率的15倍。相比之下，受tsA突变体感染的细胞不会过量产生晚期RNA。我们认为，A蛋白通过对基因A转录的负反馈控制来调节其自身的合成。
