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菌体F21的受体结合蛋白通过破坏稳定的突变演变新的功能,从而产生非遗传的表型异质性
Krista R Gerbino1, Joshua M Borin1, Sarah M Ardell1
1School of Biological Sciences, University of California San Diego, 9500 Gilman Dr, La Jolla, CA 92093, United States.
Virus evolution
|August 22, 2024
概括
病毒通过突变扩大宿主范围,破坏受体结合蛋白的稳定,从而导致各种粒子稳定性. 这种非遗传变异驱动病毒进化和宿主跳跃能力.
科学领域:
- 病毒学 病毒学
- 分子生物学分子生物学
- 进化生物学 进化生物学
背景情况:
- 病毒宿主范围的扩大对于预测流行病至关重要.
- 病毒受体结合蛋白中的少数突变可以使宿主范围扩大.
- 之前对菌体 λ 的研究表明,破坏稳定的突变导致新型受体使用,但稳定性降低.
研究的目的:
- 研究病毒是否通过破坏受体结合蛋白的稳定来扩大宿主范围,类似于细菌 λ.
- 探索菌体21 (Φ21) 主体范围扩张背后的分子机制.
- 了解非遗传异质性在病毒进化中的作用.
主要方法:
- 细菌21 (Φ21) 的实验室进化,以获得新的宿主受体.
- 测量F21及其进化后代的热力学稳定性.
- 对病毒粒子热稳定性的非遗传异质性的分析.
- 在 Φ21 感染期间操纵伴侣蛋白表达.
主要成果:
- Φ21在两个星期内进化使用了两个新的宿主受体.
- 进化的F21显示热力学稳定性下降,产生基因相同但热稳定性变异的粒子.
- 增加受体使用能力与粒子稳定性降低和更快的衰变相关.
- 受体使用的异质性在蛋白质折叠过程中出现,受蛋白质陪伴者的影响.
结论:
- 病毒宿主范围的扩张可以通过突变发生,这种突变会破坏受体结合蛋白的稳定.
- 病毒粒子稳定性的非遗传异质性与新型受体使用演变有关.
- 蛋白质折叠和伴侣活动在产生这种异质性方面发挥着作用,促进病毒适应.
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