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Rewiring Host Lipid Metabolism by Large Viruses Determines the Fate of Emiliania huxleyi, a Bloom-Forming Alga in the Ocean

机译:通过大病毒重新引导宿主脂质代谢决定了Emiliaania huxleyi的命运,Emiliania huxleyi是海洋中形成花粉的藻类

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摘要

Marine viruses are major ecological and evolutionary drivers of microbial food webs regulating the fate of carbon in the ocean. We combined transcriptomic and metabolomic analyses to explore the cellular pathways mediating the interaction between the bloom-forming coccolithophore Emiliania huxleyi and its specific coccolithoviruses (E. huxleyi virus [EhV]). We show that EhV induces profound transcriptome remodeling targeted toward fatty acid synthesis to support viral assembly. A metabolic shift toward production of viral-derived sphingolipids was detected during infection and coincided with downregulation of host de novo sphingolipid genes and induction of the viral-encoded homologous pathway. The depletion of host-specific sterols during lytic infection and their detection in purified virions revealed their novel role in viral life cycle. We identify an essential function of the mevalonate-isoprenoid branch of sterol biosynthesis during infection and propose its downregulation as an antiviral mechanism. We demonstrate how viral replication depends on the hijacking of host lipid metabolism during the chemical "arms race" in the ocean.
机译:海洋病毒是调节海洋中碳命运的微生物食物网的主要生态和进化驱动力。我们结合转录组学和代谢组学分析来探索介导绽放形成球石藻Emiliania huxleyi与其特有的球石病毒(E. huxleyi病毒[EhV])之间相互作用的细胞途径。我们表明,EhV诱导针对脂肪酸合成以支持病毒组装的深刻转录组重塑。在感染过程中检测到代谢向病毒源性鞘脂产生的转变,并与宿主新鞘氨醇基因的下调和病毒编码同源途径的诱导相吻合。溶菌感染过程中宿主特异性固醇的耗竭及其在纯化病毒粒子中的检测揭示了它们在病毒生命周期中的新作用。我们确定了固醇的甲羟戊酸-异戊二烯分枝感染过程中的基本功能,并提出其下调作为一种抗病毒机制。我们证明了病毒复制如何取决于海洋化学“军备竞赛”期间宿主脂质代谢的劫持。

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