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首页> 外文期刊>Journal of proteome research >Cellular Responses Associated with ROS Production and Cell Fate Decision in Early Stress Response to Iron Limitation in the Diatom Thalassiosira pseudonana
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Cellular Responses Associated with ROS Production and Cell Fate Decision in Early Stress Response to Iron Limitation in the Diatom Thalassiosira pseudonana

机译:与ROS产生和细胞命运决定相关的细胞响应在硅藻Thalassiosira pseudonana对铁限制的早期胁迫响应中

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摘要

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.
机译:研究硅藻如何应对海洋环境中铁生物利用度的快速波动可能有助于更好地了解其生态学成功的基础机制,尤其是它们在有利条件下快速繁殖的能力。在这项研究中,使用体内生化标记和基于全细胞iTRAQ的蛋白质组学分析,我们探索了在中心硅藻Thalassiosira pseudonana对Fe限制的早期响应过程中,与活性氧(ROS)产生和细胞命运决定相关的细胞响应。铁的限制导致光系统(PS)II的光合作用效率显着下降,PS I中光合电子传输链的损坏以及复合物III和IV中呼吸链的阻塞,所有这些都可能导致过量的ROS积累。 ROS的增加可能通过合成参与生存前和生存前因素之间微妙平衡的一系列蛋白质,在某些Fe受限的细胞中触发了程序性细胞死亡(PCD)。结果为分子假单胞菌可能对Fe限制所采用的主要策略提供了分子水平的见解:通过PCD降低细胞群体密度以减少对可用Fe的竞争,重新分配细胞内氮和Fe以确保生存,并增加抗氧化剂和抗PCD蛋白的表达以应对压力。

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