Department of Chemistry and Biochemistry, University of California, Los Angeles, California 90095-1569, USA.
Plant Cell. 2012 Jun;24(6):2649-65. doi: 10.1105/tpc.112.098962. Epub 2012 Jun 8.
Fe deficiency is one of several abiotic stresses that impacts plant metabolism because of the loss of function of Fe-containing enzymes in chloroplasts and mitochondria, including cytochromes, FeS proteins, and Fe superoxide dismutase (FeSOD). Two pathways increase the capacity of the Chlamydomonas reinhardtii chloroplast to detoxify superoxide during Fe limitation stress. In one pathway, MSD3 is upregulated at the transcriptional level up to 10(3)-fold in response to Fe limitation, leading to synthesis of a previously undiscovered plastid-specific MnSOD whose identity we validated immunochemically. In a second pathway, the plastid FeSOD is preferentially retained over other abundant Fe proteins, heme-containing cytochrome f, diiron magnesium protoporphyrin monomethyl ester cyclase, and Fe2S2-containing ferredoxin, demonstrating prioritized allocation of Fe within the chloroplast. Maintenance of FeSOD occurs, after an initial phase of degradation, by de novo resynthesis in the absence of extracellular Fe, suggesting the operation of salvage mechanisms for intracellular recycling and reallocation.
铁缺乏是影响植物代谢的几种非生物胁迫之一，因为叶绿体和线粒体中铁酶的功能丧失，包括细胞色素、Fe-S 蛋白和 Fe 超氧化物歧化酶 (FeSOD)。在铁限制胁迫期间，两种途径可提高莱茵衣藻叶绿体清除超氧阴离子的能力。在一种途径中，MSD3 在转录水平上调高达 10(3)倍，以响应铁限制，导致以前未发现的质体特异性 MnSOD 的合成，我们通过免疫化学验证了其身份。在第二种途径中，质体 FeSOD 优先保留，而不是其他丰富的铁蛋白，如含铁细胞色素 f、二铁镁原卟啉甲酯环化酶和含 Fe2S2 的铁氧还蛋白，表明铁在叶绿体中的优先分配。在没有细胞外铁的情况下，通过从头合成来维持 FeSOD 的存在，这表明存在用于细胞内回收和再分配的挽救机制。
