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Published on November 3, 2006; 10.1104/pp.106.088609

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Received August 21, 2006
Accepted October 28, 2006

Manganese Deficiency in Chlamydomonas Results in Loss of PSII and MnSOD Function, Sensitivity to Peroxides, and Secondary Phosphorus- and Iron-deficiency

Michael D. Allen , Janette Kropat , Stephen Tottey , José A. Del Campo , and Sabeeha S. Merchant *

Department of Chemistry and Biochemistry, UCLA, Box 951569, Los Angeles, CA 90095-1569

* Corresponding author; email: merchant{at}chem.ucla.edu.

For photoheterotrophic growth, a Chlamydomonas reinhardtii cell requires at least 1.7 x 107 manganese ions in the medium. At lower manganese ion concentrations (typically <0.5 µM), cells divide more slowly, accumulate less chlorophyll, and the culture reaches stationary phase at lower cell density. Below 0.1 µM supplemental manganese ion in the medium, the cells are photosynthetically defective. This is accompanied by decreased abundance of D1, which binds the Mn4Ca cluster, and release of the OEE proteins from the membrane. Assay of Mn-containing superoxide dismutase (MnSOD), indicates loss of activity of two isozymes in proportion to the Mn-deficiency. The expression of MSD3 through MSD5, encoding various isoforms of the MnSODs, is up-regulated several fold in Mn-deficient cells, but neither expression nor activity of the plastid Fe-containing superoxide dismutase (FeSOD) is changed, which contrasts with the dramatically increased MSD3 expression and plastid MnSOD activity in Fe-deficient cells. Mn-deficient cells are selectively sensitive to peroxide, but not paraquat or Rose Bengal, and GPXs, APX and MSRA2 genes are slightly up-regulated. Elemental analysis indicates that the Mn, Fe and P contents of cells in the Mn-deficient cultures were reduced in proportion to the deficiency. An NRAMP homologue and one of five MTPs were induced in Mn-deficient cells but not in Fe-deficient cells, suggesting that the corresponding gene products may be components of a Mn2+-selective assimilation pathway.




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