Manganese deficiency in Chlamydomonas results in loss of photosystem II and MnSOD function, sensitivity to peroxides, and secondary phosphorus and iron deficiency
Manganese deficiency in Chlamydomonas results in loss of photosystem II and MnSOD function, sensitivity to peroxides, and secondary phosphorus and iron deficiency
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DOI：
10.1104/pp.106.088609
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发表时间：
2007-01-01
期刊：
影响因子：
7.4
通讯作者：
Merchant, Sabeeha S.
中科院分区：
文献类型：
--
作者：
Allen, Michael D.;Kropat, Janette;Merchant, Sabeeha S.
对于光异养生长，莱茵衣藻细胞需要至少1.7 × 10（7）锰离子在培养基中。在较低的锰离子浓度（通常< 0.5 μ M）下，细胞分裂更慢，积累更少的叶绿素，并且培养物在较低的细胞密度下达到稳定期。培养基中锰离子添加量低于0.1 μ M时，细胞的光合作用有缺陷.这伴随着结合Mn4Ca簇的D1丰度的降低，以及OEE蛋白从膜的释放。锰超氧化物歧化酶（MnSOD）的测定表明两种同工酶的活性损失与锰缺乏成比例。MSD3通过MSD5的表达，编码各种亚型的MnSOD，在锰缺乏细胞中上调几倍，但无论是表达还是活性的质体含铁超氧化物歧化酶的变化，这与显着增加MSD3的表达和质体MnSOD活性在铁缺乏细胞形成对比。锰缺乏细胞对过氧化物选择性敏感，但对甲基紫精或玫瑰红不敏感，GPX、APX和MSRA2基因（编码谷胱甘肽过氧化物酶、抗坏血酸过氧化物酶和甲硫氨酸亚砜还原酶2）略微上调。元素分析表明，锰，铁，磷含量的细胞在锰缺乏的文化减少成比例的缺陷。一个天然的抗性相关的巨噬细胞蛋白同源物和五个金属耐受蛋白之一，在锰缺乏的细胞，但不是在铁缺乏的细胞诱导，这表明相应的基因产物可能是Mn2+选择性同化途径的组成部分。
For photoheterotrophic growth, a Chlamydomonas reinhardtii cell requires at least 1.7 x 10(7) manganese ions in the medium. At lower manganese ion concentrations (typically < 0.5 mu M), cells divide more slowly, accumulate less chlorophyll, and the culture reaches stationary phase at lower cell density. Below 0.1 mu M 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 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 severalfold in Mn-deficient cells, but neither expression nor activity of the plastid Fe-containing superoxide dismutase 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 methyl viologen or Rose Bengal, and GPXs, APX, and MSRA2 genes (encoding glutathione peroxidase, ascorbate peroxidase, and methionine sulfoxide reductase 2) 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. A natural resistance-associated macrophage protein homolog and one of five metal tolerance proteins 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.