Department of Biological Sciences, University of Alberta, Edmonton, Alberta, T6G 2E9, Canada.
Sci Rep. 2019 Mar 21;9(1):5215. doi: 10.1038/s41598-018-36847-6.
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.
模式颗石藻埃玛藻（Emiliania huxleyi）形成了由钙化细胞类型主导的广阔藻华，这些细胞会产生称为颗石的方解石鳞片。藻华持续数周，之后钙化藻类细胞迅速死亡，沉入深海。埃玛藻藻华的崩溃归因于感染和杀死钙化细胞的埃玛藻病毒（EhVs），而其他埃玛藻病原体，如属于玫瑰杆菌群的细菌，则被忽视了。EhVs 通过诱导产生生物活性的病毒糖脂（vGSLs）来杀死钙化的埃玛藻，从而引发藻类程序性细胞死亡（PCD）。最近发现玫瑰杆菌属的抑制菌（Phaeobacter inhibens）与钙化的埃玛藻细胞相互作用并杀死它们，但藻类死亡的机制仍不清楚。在这里，我们证明抑制菌通过诱导一种称为凋亡样程序性细胞死亡（AL-PCD）的高度特异性 PCD 来杀死钙化的埃玛藻。在存在泛半胱天冬酶抑制剂的情况下，宿主死亡可以成功被抑制，该抑制剂阻止了半胱天冬酶样分子的激活。这一发现将抑制菌和 EhV 引起的埃玛藻发病机制区分开来，证明了细菌诱导的 AL-PCD 需要活性半胱天冬酶样分子，而病毒病原体则不需要。这是首次证明细菌作为一种杀伤机制在藻类宿主中诱导 AL-PCD。
