Rewiring Host Lipid Metabolism by Large Viruses Determines the Fate of Emiliania huxleyi, a Bloom-Forming Alga in the Ocean    . Issue 6 (10th June 2014)

• Record Type: Journal Article
• Authors: Rosenwasser, Shilo; Mausz, Michaela A.; Schatz, Daniella; Sheyn, Uri; Malitsky, Sergey; Aharoni, Asaph; Weinstock, Eyal; Tzfadia, Oren; Ben-Dor, Shifra; Feldmesser, Ester; Pohnert, Georg; Vardi, Assaf
• Is Part Of: The Plant Cell. Volume 26:Issue 6(2014)
• Page Start: 2689
• Page End: 2707
• Publication Date: 2014-06-10
• DOI: 10.1105/tpc.114.125641
• Languages: English
• ISSNs: 1040-4651

Abstract

Abstract : This study investigated the interaction between the bloom-forming alga Emiliania huxleyi and its specific large virus (EhV) using RNA-seq of the host and virus coupled with metabolomic analyses. Remodeling of host lipid metabolism during infection is revealed. This is mediated, in part, by viral-encoded enzymes for sphingolipid biosynthesis, which are central to the chemical arms race at sea. Abstract: 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.