Autoregulation of simian virus 40 gene A by T antigen.
Autoregulation of simian virus 40 gene A by T antigen.
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T抗原对猿猴病毒40基因A的自动调节。
DOI：
10.1073/pnas.73.9.3083
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发表时间：
1976
影响因子：
11.1
通讯作者：
J. Alwine
中科院分区：
文献类型：
--
作者：
S. Reed;G. Stark;J. Alwine
在猿猴病毒 40 的裂解感染过程中，基因 A 转录成早期 RNA，然后翻译成 A 蛋白（T 抗原）。温度敏感A（tsA）突变体感染的细胞中早期RNA的合成速率和细胞内量均高于野生型病毒感染的细胞。这些差异在允许温度（32 度）下观察到，并且在转移到限制温度（41 度）后大大放大。例如，在 32 度时，被 tsA 突变体感染的细胞合成早期 RNA 的速度大约是被野生型病毒感染的细胞的两倍。转变至 41 度后，tsA 感染中的合成速率增加至野生型感染中的 15 倍。相反，被 tsA 突变体感染的细胞不会过量产生晚期 RNA。我们认为A蛋白通过基因A转录的负反馈控制来调节其自身的合成。
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.