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阿坎萨摩巴多菌的de novo转录组及其在Mimivirus感染期间的动态

Reut Bickels Nuri¹, Ester Feldmesser², Yael Fridmann-Sirkis³

¹Departments of Chemical and Structural Biology and Biomolecular Sciences, Weizmann Institute of Science, 7610001, Rehovot, Israel. reutnuri@gmail.com.

Scientific reports

|October 30, 2024

概括

阿坎萨莫巴菌的米米病毒感染通过改变基因表达导致宿主细胞循环停止. 病毒操纵宿主通路,包括细胞骨和过氧体,用于其复制.

科学领域:

微生物学微生物学
病毒学病毒学
细胞生物学细胞生物学

背景情况:

米米病毒 (Mimivirus bradfordmassiliense) 是一种巨型病毒,感染原生虫机会性病原体阿坎萨摩巴.
了解宿主-病毒相互作用对于破译病毒病原性至关重要.

研究的目的:

在Mimivirus感染期间描述宿主和病毒转录组动态.
阐明了Mimivirus诱导的宿主细胞修饰背后的分子机制.

主要方法:

使用长和短读数测序对Acanthamoeba进行de novo转录组组装.
在整个感染过程中对宿主和病毒基因表达的转录组分析.
功能丰富分析和细胞循环停止的实验验证.

主要成果:

主体转录组分析揭示了细胞骨恒常性和DNA复制中的下调基因,表明细胞循环停止.
观察到参与转录,分泌途径,过氧体和泛素-蛋白体系统的宿主基因的升级.
病毒基因表达从感染早期的复制相关基因转移到代谢和蛋白酶基因.
有证据表明,米米病毒会拆解宿主细胞骨,并将细胞内网膜重定向到病毒工厂.

结论:

仿真病毒感染诱导了显著的宿主细胞循环停止和代谢重编程.
病毒劫持了宿主细胞机械,包括过氧体和无素-蛋白体系统,用于其复制.
转录基因分析提供了关于Mimivirus及其宿主Acanthamoeba之间的复杂相互作用的见解.

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