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Cassidy R Prince1, Isabella N Lin1, Heather A Feaga1
1Department of Microbiology, Cornell University, Ithaca, NY 14853.
bioRxiv : the preprint server for biology
|October 10, 2024
概括
细菌翻译终结依赖于释放因子2 (RF2),该释放因子由prfB基因中的被编程的核糖体框架转移调节. 这种位转移可以防止RF2在各种细菌物种中过度表达.
科学领域:
- 分子生物学分子生物学
- 基因组学就是基因组学.
- 细菌遗传学 细菌遗传学
背景情况:
- 释放因子2 (RF2) 终止了细菌的翻译.
- 编码RF2的prfB基因需要一个被编程的核糖体框架转移来实现全长翻译,这是由于过早停止的代码.
- 对RF2水平的自我调节对于预防细胞毒性至关重要.
研究的目的:
- 研究prfB在细菌中编程的核糖体框架转移的多样性和进化模式.
- 确定prfB框架转移在自调节RF2水平中的作用.
- 了解移动动机图缺失或低效的含义.
主要方法:
- 对超过12,000个细菌基因组的生物信息分析.
- 进行比较基因组学,以识别prfB位移动动机,并阻止代码子的使用.
- 在Bacillus subtilis和Mycobacterium smegmatis中进行实验验证.
主要成果:
- prfB框架转移在细菌中很普遍,作为一种自我调节机制.
- 存在RF2特异性停止编码子 (TGA,TAA) 和没有RF1特异性编码子 (TAG) 支持自我调节.
- 缺乏框架转移的物种表现出更高的RF2停止密码子使用率,这表明需要更高的RF2水平.
- 在不进行框架转移的情况下,prfB的过度表达对 Bacillus subtilis 有毒.
- 雅基诺细菌通常缺乏prfB框架转移,在Mycobacterium smegmatis中观察到的效率较低.
结论:
- 细菌prfB编程的框架转移是一种进化保存的自我调节机制.
- 这种机制可以防止释放因子2的有毒过度表达.
- 框架转移使用的变化与细菌RF2要求和毒性值相关.
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