在解码哺乳动物甲素脱碳酶抗酶的自我调节框架转移
S Matsufuji1, T Matsufuji, Y Miyazaki
1Howard Hughes Medical Institute, University of Utah, Salt Lake City 84112.
Cell
|January 13, 1995
概括
鼠类抗酶基因表达依赖于被编程的核糖体框架转移,由聚胺水平调节. 这种自我调节机制通过降解甲氨酸脱碳酶来控制聚胺合成.
科学领域:
- 分子生物学分子生物学
- 基因规则 基因规则
- 生物化学 生物化学
背景情况:
- 鼠类抗酶基因表达是通过编程的核糖体框架转移来调节的.
- 多氨酸是参与细胞生长和增殖的必需分子.
- 甲尼丁脱碳酶是聚胺合成中的一个关键酶.
研究的目的:
- 阐明控制大鼠抗酶基因表达的新型自我调节机制.
- 调查聚氨酸在调节核糖体框架转移中的作用.
- 描述移位点及其相关序列.
主要方法:
- 在体外实验中使用网细胞溶解物进行实验.
- 融合结构的建造,以研究移效率.
- 分析mRNA序列,包括终结和下游伪结.
主要成果:
- 多氨基,特别是精子胺,以度依赖的方式调节移效率 (19%在最佳度).
- 一个+1框架转移发生在启动框架的终结器编码子的上游.
- 终端编码子和下游的伪结刺激了移动.
- 框架移位序列 (UCC-UGA-U) 是独一无二的,可能涉及超出tRNA重新配对的新机制.
结论:
- 鼠类抗酶基因表达是由多胺依赖的核糖体框架转移机制自我调节的.
- 这种机制通过控制抗酶合成来微调聚胺水平.
- 独特的移位点表明了翻译控制的新机制,包括读取或封闭第四个基点.
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