Two mechanisms for maintenance of superoxide dismutase capacity in iron deficient Chlamydomonas reinhardtii
M. Dudley Page, Michael D. Allen, Eugen Urzica, Janette Kropat, Steven Karpowitz and Sabeeha S. Merchant
Chemistry and Biochemistry, UCLA, 607 Charles E. Young Dr. E, Los Angeles, CA 90034, USA
Two pathways increase the capacity of the chloroplast to detoxify superoxide during iron limitation stress. In one pathway, the MSD3 gene, encoding a plastid-specific MnSOD (one of 5 MnSODs in C. reinhardtii) is dramatically upregulated, up to 1000-fold, at the transcriptional level, in response to iron limitation. In a second pathway, the plastid FeSOD is preferentially retained over cytochrome f, the CTH1 diiron Mg-PPMME cyclase, and ferredoxin, which are degraded during iron limitation. Maintenance of FeSOD occurs, after an initial phase of degradation, by de novo resynthesis in the absence of extracellular iron, suggesting a mechanism for recycling and for prioritized allocation of iron.
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