Overexpression of Arabidopsis ATX1 retards plant growth under severe copper deficiency.

In a previous study, we demonstrated that Arabidopsis Antioxidant Protein1 (ATX1) plays an essential role in copper (Cu) homeostasis, conferring tolerance to both excess and subclinically deficient Cu. The Cu-binding motif MXCXXC was required for the physiological function of ATX1. In this study, we found that overexpression of ATX1 resulted in hypersensitivity to severe Cu deficiency despite enhancing tolerance to subclinical Cu deficiency. However, overexpression of mutated ATX1, replacing the Cu-binding motif MXCXXC with MXGXXG, abolished the hypersensitivity, for no differences from the wild type under the same conditions. Thus, the expression of ATX1 must be cautiously regulated to avoid homeostatic imbalance with the over-chelation of Cu.

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