概括
分析了Rous瘤病毒的src基因中的两个突变. 一个框架转移突变导致了逆转,而重复抑制了它,恢复了SRC蛋白质合成.
科学领域:
- 分子生物学分子生物学
- 病毒学 病毒学
- 癌症研究 癌症研究
背景情况:
- 鼠肉瘤病毒 (RSV) 对老鼠细胞的转化导致表型变化.
- 对SRC基因突变的分析对于理解病毒瘤发生至关重要.
研究的目的:
- 在RSV转化老鼠细胞中研究表型逆转和逆转的分子机制.
- 为了表征负责这些细胞变化的 src 基因内的突变.
主要方法:
- 从复原和转化细胞系中克隆的前病毒DNA的核酸测序.
- 使用分子量估计 (kd) 来分析src蛋白产品.
主要成果:
- 一个单个基对插入逆向线000的src基因引起了一个框架转移突变,产生了一个18kd的截断src蛋白.
- 在重新转换的线000*中进行了242bp的重复,纠正了移,允许合成68kd src蛋白.
- 这两种细胞系都产生了由内部AUG启动的43kd src蛋白,这表明从同一mRNA开始独立翻译.
结论:
- 在SRC中的框架转移突变可以通过改变蛋白质产品导致表型逆转.
- 复制可以抑制移突变,恢复功能性SRC蛋白和转化.
- RSV src基因可以通过替代的翻译启动站点和阅读框架产生多种蛋白质异型.
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