An Examination of the Autocatalytic Cell Death Machinery in Marine, Planktonic Photoautotrophs

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Phytoplankton mortality largely determines how other organisms live and is essential to linking major biogeochemical cycles in the ocean. Unfortunately, the mechanisms controlling the dramatic and abrupt bloom termination in natural systems are not well understood. Like all marine organisms, microscopic phytoplankton encounter adverse environmental conditions in the ocean (i.e., nutrient stress), which result in physiological stress and, sometimes, death. Indeed, substantial cell death (via lysis) has been documented in field studies with some estimates exceeding 50% of phytoplankton growth. This proposal examines autocatalyzed cell death in marine phytoplankton, a self-destruction analogous to programmed cell death (PCD) or apoptosis in multicellular organisms. It focuses (1) on the ecological relevance of PCD as a critical mortality mechanism of phytoplankton in response to environmental stress and (2) on the origins of PCD in marine phytoplankton by examining its cellular machinery and their relationship to those employed by multicellular organisms, for which this type of death in best understood. Proposed research examines PCD pathways in diverse lineages of phytoplankton, including a cyanobacterium (Trichodesmium sp. IMS101), a chlorophyte (Dunaliella tertiolecta) and a coccolithophorid (Emiliania huxleyi). Based on preliminary findings, similar PCD pathways appear to be activated in these organisms in response to physiological and environmental stress (culture age, oxidative stress, iron and phosphorus limitation), each resulting in massive cell death. It specifically addresses whether a specific class of proteases, termed Caspases, activate and execute PCD in phytoplankton. Caspases play a ubiquitous role in the execution of PCD in metazoans, functioning both in cell disassembly (effectors) and in initiating this disassembly (initiators). In addition, this proposal investigates whether the PCD cellular machinery is activated upon viral infection of phytoplankton, using E. huxleyi and its virus (EhV1) as a model system. In metazoans (e.g., humans), PCD is often employed as a defense mechanism by host cells to prevent spread of viral infection. The PCD machinery may have evolved in phytoplankton to prevent massive viral infection and demise of natural populations.This research will provide a variety of broader impacts. Research findings will provide critical mechanistic insight into phytoplankton mortality as well as novel ecological and evolutionary context for PCD. Research activities will provide hands-on training for development of an undergraduate student and help to broaden the participation of underrepresented groups such as women and minorities. It will also establish collaboration between Rutgers, a leading research institute, and Cal State University San Marcos, a new minority serving institution with a strong educational mission. In collaboration with the education staff at the Institute of Marine and Coastal Science (Rutgers University), research findings will be translated for K-12 and public audiences in New Jersey, as part of the newly established, NSF-funded Mid-Atlantic Center for Ocean Science Education Excellence (MA-COSEE).