Cellular Responses Associated with ROS Production and Cell Fate Decision in Early Stress Response to Iron Limitation in the Diatom Thalassiosira pseudonana

Investigation of how diatoms cope with the rapid fluctuations in iron bioavailability in marine environments may facilitate a better understanding of the mechanisms underlying their ecological success, in particular their ability to proliferate rapidly during favorable conditions. In this study, using in vivo biochemical markers and whole-cell iTRAQ-based proteomics analysis, we explored the cellular responses associated with reactive oxygen species (ROS) production and cell fate decision during the early response to Fe limitation in the centric diatom Thalassiosira pseudonana. Fe limitation caused a significant decrease in Photosystem (PS) II photosynthetic efficiency, damage to the photosynthetic electron transport chain in PS I, and blockage of the respiratory chain in complexes III and IV, which could all result in excess ROS accumulation. The increase in ROS likely triggered programmed cell death (PCD) in some of the Fe-limited cells through synthesis of a series of proteins involved in the delicate balance between pro-survival and pro-PCD factors. The results provide molecular-level insights into the major strategies that may be employed by T. pseudonana in response to Fe-limitation: the reduction of cell population density through PCD to reduce competition for available Fe, the reallocation of intracellular nitrogen and Fe to ensure survival, and an increase in expression of antioxidant and anti-PCD proteins to cope with stress.

探究硅藻如何应对海洋环境中铁生物利用度的快速波动，有助于更深入阐明其生态成功背后的核心机制，尤其是其在适宜条件下快速增殖的能力。本研究以中心硅藻假微型海链藻（Thalassiosira pseudonana）为实验材料，采用体内生化标记物与全细胞iTRAQ标记蛋白质组学分析技术，探究了其在铁限制早期响应过程中与活性氧（reactive oxygen species, ROS）生成及细胞命运决定相关的细胞应答反应。铁限制会显著降低光系统II（PS II）的光合效率，损伤光系统I（PS I）中的光合电子传递链，并阻断复合体III与IV中的呼吸链，上述变化均可引发活性氧过量积累。活性氧水平升高可能通过合成一系列参与调控促存活与促细胞程序性死亡（programmed cell death, PCD）因子间精细平衡的蛋白质，触发部分铁限制细胞发生细胞程序性死亡。本研究结果从分子层面揭示了假微型海链藻应对铁限制的核心策略：通过细胞程序性死亡降低细胞种群密度以减少对有限铁元素的竞争，重新分配细胞内氮与铁以保障存活，并上调抗氧化与抗细胞程序性死亡蛋白的表达以应对胁迫。