Cytosolic fumarase acts as a metabolic fail-safe for both high and low temperature acclimation of Arabidopsis thaliana.
Cytosolic fumarase acts as a metabolic fail-safe for both high and low temperature acclimation of Arabidopsis thaliana.
复制标题
胞质延胡索酸酶对于拟南芥的高温和低温驯化起着代谢故障保护作用。
DOI：
10.1093/jxb/erab560
复制
发表时间：
2022
影响因子：
6.9
通讯作者：
Saunders HA
中科院分区：
文献类型：
--
作者：
Saunders HA
植物调整其光合能力以适应不断变化的环境条件。在拟南芥中，光合作用对寒冷的适应需要富马酸有机酸的积累，由胞质富马酸酶FUM2催化。然而，这种积累的作用目前尚不清楚。在这项研究中，我们使用综合实验和建模方法来检查富马酸和富马酸在生理温度范围内的作用。通过生理生化分析，我们证明了在高温和低温驯化中，FUM2都是必需的。我们采用了一种可靠性工程技术，失效模式和影响分析（FMEA），根据代谢物对代谢系统构成的潜在风险，制定了一种严格的方法来对代谢物进行排名。FMEA将富马酸确定为低风险代谢物，而其前体苹果酸被证明是高风险的，容易导致系统不稳定。我们得出的结论是，胞质延胡索酸酶（FUM2）的作用是提供故障安全，控制苹果酸浓度，在不断变化的环境中保持系统稳定性。我们认为FMEA是一种不仅对了解植物代谢有用的技术，而且可以用于研究其他系统和合成途径的可靠性。
Plants acclimate their photosynthetic capacity in response to changing environmental conditions. InArabidopsis thaliana,photosynthetic acclimation to cold requires the accumulation of the organic acid fumarate, catalysed by a cytosolic fumarase FUM2. However, the role of this accumulation is currently unknown. In this study, we use an integrated experimental and modelling approach to examine the role of FUM2 and fumarate across the physiological temperature range. Using physiological and biochemical analyses, we demonstrate that FUM2 is necessary for high as well as low temperature acclimation. We have adapted a reliability engineering technique, Failure Mode and Effect Analysis (FMEA), to formalize a rigorous approach for ranking metabolites according to the potential risk that they pose to the metabolic system. FMEA identifies fumarate as a low-risk metabolite, while its precursor, malate, is shown to be high-risk and liable to cause system instability. We conclude that the role of cytosolic fumarase, FUM2, is to provide a fail-safe, controlling malate concentration, maintaining system stability in a changing environment. We argue that FMEA is a technique that is not only useful in understanding plant metabolism but can also be used to study reliability in other systems and synthetic pathways.