Expression of a dye-decolorizing peroxidase results in hypersensitive response to cadmium stress through reducing the ROS signal in Arabidopsis

• Expression of a new DyP-type peroxidase, GlDyP, was induced by oxidative stress.
• Transient induction of GlDyP was associated with abiotic stress tolerance.
• Transgenic plants constitutively expressing GlDyP reduced ROS signal.
• Transgenic plants exhibited hypersensitive response to heavy metal.
• GlDyP potentially functions in reduction of oxidative damage in Ganoderma mycelium.

Dye-decolorizing peroxidase (DyP) exhibits high activity in the degradation of textile dyes. In this study, a new DyP was isolated from Ganoderma lucidum (designated as GlDyP) that exhibits similarities to DyP in Thanatephorus cucumeris Dec1. The GlDyP expression was transiently induced by stress due to exposure to H2O2, heavy metal ions Cd2+ and Cu2+, and osmotic pressure. Consistent with the induction of GlDyP expression, the mycelium growth exhibited increased tolerance to these specific stress factors. Heavy metal Zn2+ ions caused no change in GlDyP expression; however, high salinity resulted in a reduction of GlDyP expression. Accordingly, mycelium growth exhibited unaltered tolerance to Zn2+ ions and a hypersensitive response to NaCl. Heterogeneous expression of GlDyP in Arabidopsis resulted in reduced H2O2 concentration and decreased protein accumulation of the antioxidant enzyme ascorbate peroxidase. Transcriptome analysis revealed that genes involved in oxidation reduction, the defense response, transcription regulation and the ethylene signaling pathway were significantly down-regulated in transgenic plants. Moreover, transgenic seedlings exhibited phenotypes of reduced stature with a hypersensitive response to Cd2+ ions. Altogether, the results of this study suggest the involvement of GlDyP in the regulation of reactive oxygen species (ROS) signals in G. lucidum. However, constitutive GlDyP expression can impair the defense response against cadmium stress due to the generation of insufficient ROS signals.