Final Activity Report Summary - APINOD (Functions of antioxidants and peroxide in legume nodule development)
Legume nodules are symbiotic structures formed by the molecular interaction between rhizobia and plant roots. Nodules contain antioxidant enzymes and metabolites to protect N2 fixation from reactive oxygen species. Superoxide dismutases (SODs) are metalloenzymes that play a primary role in the protection against oxidative stress in plants and other organisms. We have characterised four SOD genes in Lotus japonicus and have analysed their expression in roots and four developmental stages of nodules.
The expression of cytosolic CuZnSOD, at the mRNA, protein, and enzyme activity levels, decreases with nodule age, and the protein is localised in the dividing cells and infection threads of emergent nodules, and in cytosol of the infected cells of young nodules. The mitochondrial MnSOD gene was downregulated, whereas the bacteroidal MnSOD gene had maximal protein and enzyme activity levels in older nodules. Two additional genes, encoding plastidic (FeSOD1) and cytosolic (FeSOD2) FeSOD isoforms, were identified and mapped. The genes are located in different chromosomes and show differential expression. The FeSOD1 mRNA level did not change during nodule development, whereas FeSOD2 was upregulated. The distinct expression patterns of the SOD genes may reflect different regulatory mechanisms of the enzyme activities during nodule ontogeny. In particular, at the mRNA and activity levels, the virtual loss of cytosolic CuZnSOD in mature and old nodules, concomitant with the induction of FeSOD2, suggest that the two enzymes may functionally compensate each other in the cytosol at the late stages of nodule development.
The expression of cytosolic CuZnSOD, at the mRNA, protein, and enzyme activity levels, decreases with nodule age, and the protein is localised in the dividing cells and infection threads of emergent nodules, and in cytosol of the infected cells of young nodules. The mitochondrial MnSOD gene was downregulated, whereas the bacteroidal MnSOD gene had maximal protein and enzyme activity levels in older nodules. Two additional genes, encoding plastidic (FeSOD1) and cytosolic (FeSOD2) FeSOD isoforms, were identified and mapped. The genes are located in different chromosomes and show differential expression. The FeSOD1 mRNA level did not change during nodule development, whereas FeSOD2 was upregulated. The distinct expression patterns of the SOD genes may reflect different regulatory mechanisms of the enzyme activities during nodule ontogeny. In particular, at the mRNA and activity levels, the virtual loss of cytosolic CuZnSOD in mature and old nodules, concomitant with the induction of FeSOD2, suggest that the two enzymes may functionally compensate each other in the cytosol at the late stages of nodule development.