Abstract
The model coccolithophore, Emiliania huxleyi, forms expansive blooms dominated by the calcifying cell type, which produce calcite scales called coccoliths. Blooms last several weeks, after which the calcified algal cells rapidly die, descending into the deep ocean. E. huxleyi bloom collapse is attributed to E. huxleyi viruses (EhVs) that infect and kill calcifying cells, while other E. huxleyi pathogens, such as bacteria belonging to the roseobacter clade, are overlooked. EhVs kill calcifying E. huxleyi by inducing production of bioactive viral-glycosphingolipids (vGSLs), which trigger algal programmed cell death (PCD). The roseobacter Phaeobacter inhibens was recently shown to interact with and kill the calcifying cell type of E. huxleyi, but the mechanism of algal death remains unelucidated. Here we demonstrate that P. inhibens kills calcifying E. huxleyi by inducing a highly specific type of PCD called apoptosis-like-PCD (AL-PCD). Host death can successfully be abolished in the presence of a pan-caspase inhibitor, which prevents the activation of caspase-like molecules. This finding differentiates P. inhibens and EhV pathogenesis of E. huxleyi, by demonstrating that bacterial-induced AL-PCD requires active caspase-like molecules, while the viral pathogen does not. This is the first demonstration of a bacterium inducing AL-PCD in an algal host as a killing mechanism.
Highlights
Coccolithophores are well known for their precipitation of dissolved bicarbonate to produce characteristic ornate calcite disks or coccoliths[1]
The dramatic loss of Photosystem System II (PSII) health was suggestive of reactive oxygen species (ROS) involvement in cellular destruction, which is a notable occurrence during E. huxleyi viruses (EhVs) infection of E. huxleyi[38,39]
To monitor the proportion of algal cells with elevated intracellular ROS, the ROS indicator CM-H2DCFDA was added to algal cultures, where it was rapidly hydrolyzed by algal esterases, oxidized by ROS in the cytoplasm, resulting in intracellular fluorescent dichlorofluorescein (DCF)[38,41]
Summary
Coccolithophores are well known for their precipitation of dissolved bicarbonate to produce characteristic ornate calcite disks or coccoliths[1]. The duration of coccolithophore blooms can be dramatically shortened by predation from microzooplankton[8] and infection by viruses[9] The latter can trigger premature collapse of E. huxleyi blooms by hijacking algal PCD pathways, inducing algal death[10,11,12]. Given that lytic E. huxleyi viruses (EhVs) produce bioactive viral glycosphingolipids (vGSLs) that trigger E. huxleyi PCD11 and/or autophagy pathways[12], we hypothesized that bacterially induced AL-PCD might be the cause of algal death in this bacterial-algal interaction To test this hypothesis, E. huxleyi was grown in co-culture with P. inhibens and monitored for previously identified PCD phenotypes associated with viral infection of E. huxleyi (i.e. generation of reactive oxygen species (ROS)[38,39] and elevated caspase-like IETDase activities[11,29]). Algal cell death by AL-PCD was further confirmed by the observation of late-stage nuclear degradation and subsequent loss of cellular DNA18,21
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