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Myo-inositol is a vital compound in plants. As the key rate-limiting enzyme in myo-inositol biosynthesis, l-myo-inositol-1-phosphate synthase (MIPS) is regarded as a determinant of the myo-inositol content in plants. The up-regulation of MIPS genes can increase the myo-inositol content, thereby enhancing the plant's resistance to a variety of stresses. However, there are few reports on the roles of myo-inositol and the identification of MIPS in woody trees. In this study, a MIPS gene, named as PeMIPS1, was characterized from Populus euphratica Oliv. The heterologous expression of PeMIPS1 compensated for inositol production in the yeast inositol auxotrophic mutant ino1 and the phenotypic lesions of the atmips1-2 mutant, an Arabidopsis MIPS1 knock-out mutant. A subcellular location analysis showed that the PeMIPS1-GFP fusion was localized in the nucleus and cytoplasm, but not in the chloroplasts, indicating that PeMIPS1 represented the cytosolic form of MIPS in P. euphratica. Interestingly, PeMIPS1 was not only inducible by drought and high salinity, but also by CuSO4 treatment. The transgenic poplar lines overexpressing PeMIPS1 had greater plant heights, shoot biomasses and survival rates than the wild type during the salt- or copper-stress treatment, and this was accompanied by an increase in the myo-inositol content. The overexpression of PeMIPS1 resulted in the increased activities of antioxidant enzymes and the accumulation of ascorbate, a key nonenzymatic antioxidant in plant, which partly accounted for the enhanced reactive oxygen species-scavenging capacity and the lowered hydrogen peroxide and malondialdehyde levels in the transgenic poplar. To the best of our knowledge, this study is the first to report the roles of MIPS genes in the tolerance to copper stress.

Overexpression of PeMIPS1 confers tolerance to salt and copper stresses by scavenging reactive oxygen species in transgenic poplar