Arabidopsis HY1 confers cadmium tolerance by decreasing nitric oxide production and improving iron homeostasis.

Up-regulation of the gene that encodes intracellular heme oxygenase 1 (HO1) benefits plants under cadmium (Cd(2+)) stress; however, the molecular mechanisms remain unclear. Here, we elucidate the role of Arabidopsis HY1 (AtHO1) in Cd(2+) tolerance by using genetic and molecular approaches. Analysis of two HY1 null mutants, three HY1 overexpression lines, HO double or triple mutants, as well as phyA and phyB mutants revealed the specific hypersensitivity of hy1 to Cd(2+) stress. Supplementation with two enzymatic by-products of HY1, carbon monoxide (CO) and iron (Fe, especially), rescued the Cd(2+)-induced inhibition of primary root (PR) elongation in hy1-100. The mutation of HY1, which exhibited lower glutathione content than Col-0 in root tissues, was able to induce nitric oxide (NO) overproduction, Cd(2+) accumulation, and severe Fe deficiency in root tissues. However, the contrasting responses appeared in 35S:HY1-4. Additionally, reduced levels of Ferric Reduction Oxidase 2 (FRO2) and Iron-Regulated Transporter 1 (IRT1) transcripts, and increased levels of Heavy Metal ATPase 2/4 (HMA2/4) transcripts bolster the notion that HY1 up-regulation ameliorates Fe deficiency, and might increase Cd(2+) exclusion. Taken together, these results showed that HY1 plays a common link in Cd(2+) tolerance by decreasing NO production and improving Fe homeostasis in Arabidopsis root tissues.

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