The Arabidopsis (Arabidopsis thaliana) yellow variegated2 (var2) mutant, lacking functional FILAMENTATION TEMPERATURE-SENSITIVE H2 (FtsH2), an ATP-dependent zinc metalloprotease, is a powerful tool for studying the photosystem II (PSII) repair process in plants. FtsH2, forming hetero-hexamers with FtsH1, FtsH5, and FtsH8, plays an indispensable role in PSII proteostasis. Although abiotic stresses like cold and heat increase chloroplast reactive oxygen species (ROS) and PSII damage, var2 mutants behave like wild-type plants under heat stress but collapse under cold stress. Our study on transgenic var2 lines expressing FtsH2 variants, defective in either substrate extraction or proteolysis, reveals that cold stress causes an increase in membrane viscosity, demanding more substrate extraction power than proteolysis by FtsH2. Overexpression of FtsH2 lacking substrate extraction activity does not rescue the cold-sensitive phenotype, while overexpression of FtsH2 lacking protease activity does in var2, with other FtsH isomers present. This indicates that FtsH2's substrate extraction activity is indispensable under cold stress when membranes become more viscous. As temperatures rise and membrane fluidity increases, substrate extraction activity from other isomers suffices, explaining the var2 mutant's heat stress resilience. These findings underscore the direct effect of membrane fluidity on the functionality of the thylakoid FtsH complex under stress. Future research should explore how membrane fluidity impacts proteostasis, potentially uncovering strategies to modulate thermosensitivity.

中文翻译：

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温度驱动的膜流动性变化对细丝温度敏感 H2 介导的光系统 II 修复产生差异


拟南芥 （Arabidopsis thaliana） 黄色杂色 2 （var2） 突变体，缺乏功能性细丝温度敏感 H2 （FtsH2），一种 ATP 依赖性锌金属蛋白酶，是研究植物光系统 II （PSII） 修复过程的有力工具。FtsH2 与 FtsH1、FtsH5 和 FtsH8 形成异六聚体，在 PSII 蛋白稳态中起着不可或缺的作用。尽管冷和热等非生物胁迫会增加叶绿体活性氧 （ROS） 和 PSII 损伤，但 var2 突变体在热胁迫下表现得像野生型植物，但在冷胁迫下会崩溃。我们对表达 FtsH2 变体的转基因 var2 品系的研究显示，低温应激导致膜粘度增加，比 FtsH2 的蛋白水解需要更多的底物提取能力。过表达缺乏底物提取活性的 FtsH2 并不能挽救冷敏感的表型，而过表达缺乏蛋白酶活性的 FtsH2 在 var2 中可以， 存在其他 FtsH 异构体。这表明当膜变得更粘稠时，FtsH2 的底物提取活性在冷应激下是必不可少的。随着温度升高和膜流动性增加，其他异构体的底物提取活性就足够了，这解释了 var2 突变体的热应激弹性。这些发现强调了膜流动性对压力下类囊体 FtsH 复合物功能的直接影响。未来的研究应探索膜流动性如何影响蛋白质稳态，从而可能揭示调节热敏性的策略。