在prfB的细菌域中,编程的核糖体框架转移的保存和演变
Cassidy R Prince1, Isabella N Lin1, Heather A Feaga1
1Department of Microbiology, Cornell University, Ithaca, New York, USA.
mBio
|August 18, 2025
概括
细菌释放因子2 (RF2) 的产生是由prfB基因中的编程核糖体框架转移调节的. 这种调节动机,可能是古老的,在细菌中保存,损失与特定的停止密码子使用有关.
科学领域:
- 分子生物学分子生物学
- 细菌遗传学 细菌遗传学
- 进化生物学 进化生物学
背景情况:
- 细菌中的翻译终结依赖于释放因子RF1和RF2.
- 在许多细菌中,RF2 (prfB) 的基因需要编程的核糖体框架转移来实现全长蛋白质合成,这是由于过早停止的代码.
- 之前对这种移机制的研究范围有限.
研究的目的:
- 综合分析prfB编程的细菌域内的核糖体移模式的进化和保护.
- 为了确定与这种调节动机丧失相关的基因组特征.
- 为了研究停止子使用和RF2自调节的保存之间的关系.
主要方法:
- 对超过12,000个细菌基因组的生物信息分析.
- 在prfB图案中保存的框架转移元件的表征.
- 动机损失和RF2特异性停止密码子使用之间的相关性分析.
- 在Actinomycetota.ta.的模型生物体中进行实验验证.
主要成果:
- prfB编程的核糖体框架转移动图可能存在于细菌的最后一个共同祖先中,并且高度保存.
- 动机的丧失与高RF2特异性停止的使用有很强的相关性,特别是在Actinomycetota.中缺席.
- 过度表达的RF2从一个非移 prfB等位基因是有毒的模型生物体,表明一个健身成本.
结论:
- prfB编程的核糖体框架转移是一种广泛保存的细菌调节机制.
- 停止子使用模式显著影响这种自我调节动机的保存和丧失.
- 在缺乏高RF2特异性停止密码子的细菌中,RF2自调节提供了选择性优势.
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