The Adaptation Mechanism to Copper Deficiency via MicroRNA in Arabidopsis

Abstract

Copper is an essential micronutrient for all living organisms. However, excess copper is toxic because of a production of free radicals via the free form of copper. Therefore, copper levels must be precisely regulated in a cell. In higher plants, major copper proteins are plastocyanin localized to the thylakoid lumen of chloroplasts, and copper/zinc superoxide dismutase localized to the cytoplasm and in the chloroplast stroma. Under copper-limited conditions, expression of copper/zinc superoxide dismutase is down-regulated and its function is compensated by iron superoxide dismutase in chloroplasts. Here, we present several lines of evidence indicating that microRNA, miR398, is involved in this regulation in Arabidopsis thaliana, by directing degradation of copper/zinc superoxide dismutase mRNAs when copper is limited. This regulation via miR398 takes place in response to changes in copper concentration of less than 0.5 μM, indicating that miR398 is involved in a response to copper limitation. On the other hand, another major copper protein, plastocyanin which essential for photosynthetic electron flow in higher plants was not regulated via miR398. In low copper conditions, limited copper is preferentially transported to plastocyanin. We conclude that miR398 is a key factor in copper homeostasis in higher plants.