Phaeobacter inhibens induces apoptosis-like programmed cell death in calcifying Emiliania huxleyi

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 attr...

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Bibliographic Details
Published in:Scientific reports 2019-03, Vol.9 (1), p.5215-5215, Article 5215
Main Authors: Bramucci, Anna R., Case, Rebecca J.
Format: Article
Language:English
Subjects:
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Algae
Apoptosis
Calcite
Calcium - metabolism
Calcium carbonate
Caspase inhibitors
Cell death
Emiliania huxleyi
Glycosphingolipids
Haptophyta - metabolism
Haptophyta - microbiology
Humanities and Social Sciences
Mortality
multidisciplinary
Pathogens
Phytoplankton - metabolism
Phytoplankton - microbiology
Plankton
Rhodobacteraceae - metabolism
Science
Science (multidisciplinary)
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Summary: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.
ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-018-36847-6