Abstract
ABSTRACT
Bacterial infochemicals can profoundly alter phytoplankton physiology, yet how these compounds influence viral infection outcomes remains poorly understood. The bacterial quorum sensing molecule 2-heptyl-4-quinolone (HHQ) enables the globally abundant coccolithophore,
Gephyrocapsa huxleyi
, to evade virus-induced mortality following infection by
Emiliania huxleyi
virus (EhV). HHQ reduced infectious virus production at 24 hours despite largely intact viral gene transcription, as revealed by RNA sequencing of host and viral responses during EhV-201 infection. Host transcriptomics instead revealed rapid and progressive HHQ-dependent physiological remodeling evidenced by changes in protein encoding genes associated with vesicular trafficking, and cytoskeletal organization. Transcriptional responses further implicated endolysosomal sorting, membrane remodeling, and protein modification as potential barriers to productive infection. These findings indicate that HHQ-mediated evasion of virus-induced mortality occurs downstream of viral entry and transcription, through remodeling of host processes required for virion assembly, maturation, trafficking, and release.
IMPORTANCE
Viruses are major drivers of phytoplankton mortality in the ocean, influencing the fate of photosynthetic biomass and the movement of carbon and nutrients through marine ecosystems. Yet, the extent to which bacterial infochemicals can mechanistically alter the outcome of phytoplankton viral infections remains poorly understood. Here, we show that the bacterial signaling molecule 2-heptyl-4-quinolone alters infection of the globally important marine alga,
Gephyrocapsa huxleyi
. Rather than broadly suppressing viral gene transcription, the bacterial signal rapidly alters host processes involved in intracellular transport, protein quality control, and cytoskeletal organization. These changes may prevent infected cells from efficiently assembling, transporting, or releasing infectious viral progeny. These findings identify host physiological remodeling as a mechanism by which a bacterial chemical signal can alter the outcome of algal– virus interactions, highlighting an underappreciated role for bacterial metabolites in shaping marine viral infection and potentially the fate of phytoplankton populations.