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

海洋浮游光合自养生物自催化细胞死亡机制的检查

• 批准号: 0414536
• 负责人: Kay Bidle
• 金额: --
• 依托单位: Rutgers University New Brunswick
• 依托单位国家: 美国
• 项目类别: Standard Grant
• 财政年份: 2004
• 资助国家: 美国
• 起止时间: 2004-07-01 至 2009-08-31
• 项目状态: 已结题
• 来源: https://www.nsf.gov/awardsearch/showAward?AWD_ID=0414536&HistoricalAwards=false
• 关键词: Examination; Autocatalytic; Cell; Death; Machinery

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).

浮游植物的死亡率在很大程度上决定了其他生物的生存方式，并且对于连接海洋中的主要生物地球化学循环至关重要。 不幸的是，控制自然系统中戏剧性和突然的水华终止的机制尚不清楚。与所有海洋生物一样，微小浮游植物在海洋中遇到不利的环境条件（即营养压力），从而导致生理压力，有时甚至导致死亡。 事实上，实地研究已记录了大量的细胞死亡（通过裂解），一些估计超过了浮游植物生长的 50%。 该提案研究了海洋浮游植物中的自催化细胞死亡，这是一种类似于多细胞生物中的程序性细胞死亡（PCD）或细胞凋亡的自我毁灭。它的重点是（1）PCD作为浮游植物响应环境压力的关键死亡机制的生态相关性，以及（2）通过检查其细胞机制及其与多细胞生物所使用的细胞机制的关系来研究海洋浮游植物中PCD的起源，对于这种类型的死亡是最好理解的。 拟议的研究检查了不同浮游植物谱系的 PCD 途径，包括蓝藻 (Trichodesmium sp. IMS101)、叶绿藻 (Dunaliella tertiolecta) 和颗石藻 (Emiliania huxleyi)。根据初步发现，这些生物体中似乎会激活类似的 PCD 途径来响应生理和环境应激（培养年龄、氧化应激、铁和磷限制），每种途径都会导致大量细胞死亡。 它专门讨论了称为半胱天冬酶的特定类别的蛋白酶是否在浮游植物中激活和执行 PCD。 Caspases 在后生动物 PCD 的执行中发挥着普遍的作用，在细胞分解（效应器）和启动这种分解（启动器）中发挥作用。 此外，该提案使用赫胥黎埃里希氏菌及其病毒（EhV1）作为模型系统，研究浮游植物病毒感染时 PCD 细胞机制是否被激活。 在后生动物（例如人类）中，PCD 通常被宿主细胞用作防御机制，以防止病毒感染的传播。 PCD 机制可能在浮游植物中进化，以防止大规模病毒感染和自然种群的死亡。这项研究将提供各种更广泛的影响。 研究结果将为浮游植物死亡率提供重要的机制见解，并为 PCD 提供新的生态和进化背景。 研究活动将为本科生的发展提供实践培训，并有助于扩大妇女和少数族裔等代表性不足的群体的参与。 它还将在领先的研究机构罗格斯大学和具有强大教育使命的新的少数族裔服务机构加州州立大学圣马科斯分校之间建立合作关系。 与海洋和海岸科学研究所（罗格斯大学）的教育人员合作，研究成果将被翻译给新泽西州的 K-12 和公众受众，作为新成立的、由 NSF 资助的中大西洋中心的一部分卓越海洋科学教育 (MA-COSEE)。