The Arabidopsis DJ-1a protein confers stress protection through cytosolic SOD activation

Abstract

SummaryMutations in the DJ-1 gene (also known as PARK7) cause inherited Parkinson's disease, which is characterized by neuronal death. Although DJ-1 is thought to be an antioxidant protein, the underlying mechanism by which loss of DJ-1 function contributes to cell death is unclear. Human DJ-1 and its Arabidopsis thaliana homologue, AtDJ-1a, are evolutionarily conserved proteins, indicating a universal function. To gain further knowledge of the molecular features associated with DJ-1 dysfunction, we have characterized AtDJ1a. We show that AtDJ-1a levels are responsive to stress treatment and that AtDJ-1a loss of function results in accelerated cell death in aging plants. By contrast, transgenic plants with elevated AtDJ-1a levels have increased protection against environmental stress conditions, such as strong light, H 2 O 2 , methyl viologen and copper sulfate. We further identify superoxide dismutase 1 (SOD1) and glutathione peroxidase 2 (GPX2) as interaction partners of both AtDJ-1a and human DJ-1, and show that this interaction results in AtDJ-1a-and DJ-1-mediated cytosolic SOD1 activation in a copper-dependent fashion. Our data have highlighted a conserved molecular mechanism for DJ-1 and revealed a new protein player in the oxidative stress response of plants.

Illumination of Arabidopsis roots induces immediate burst of ROS production

“…It was previously reported that endogenous AtDJ-1 level in leaf was increased after treatment with stress factors, such as strong light, H 2 O 2 , methyl viologen and copper sulfate. 23 DJ-1 supports the cellular redox homeostasis by subserving a SOD-activity in both mammalian and plant cells. 23 Here we have found, following the GUS staining protocol of Vitha et al, 24 increased DJ-1::GUS expression in root apices of Arabidopsis in response to short (30 min) blue light exposures (Fig.…”

“…In Figure 3D, we used GUS line of Arabidopsis DJ-1 (AtDJ-1) which was identified as a homolog of Human DJ-1 PARK7. 23 Mutation of human DJ-1 causes Parkinson's disease resulting in neuronal death. It was previously reported that endogenous AtDJ-1 level in leaf was increased after treatment with stress factors, such as strong light, H 2 O 2 , methyl viologen and copper sulfate.…”

ROS removal by DJ-1

“…7,8 Therefore, Enzyme assays revealed that AtDJ-1a and DJ-1 stimulated SOD/CSD1 activity and that only the copper-loaded forms of AtDJ-1a and DJ-1 had this effect suggesting that AtDJ-1a/DJ-1 may provide copper for SOD/CSD1. 11 Although the observed SOD activation provides clues towards the role of DJ-1 in detoxification of ROS, SOD only converts superoxide anion to H 2 O 2 which must further be detoxified to H 2 O by GPX and CAT. Although we showed that AtDJ-1a and human DJ-1 can interact with AtGPX2 and GPX2, respectively, we observed no changes in GPX2 activity upon DJ-1 interaction.…”

“…The fact that Arabidopsis has three DJ-1 homologs where two of these, AtDJ-1b and AtDJ-1c, are localized to chloroplasts 11 underlines the protective has been elusive in terms of having a direct influence on neuronal cell death. 10 In an attempt to clarify the mechanism of DJ-1 we established Arabidopsis thaliana as a new and novel model system.…”

“…11 As SOD, GPX, CAT and APX, together with other auxiliary proteins, form the main line of defense against ROS. DJ-1 was originally identified as an oncogene and represents a ubiquitous redox-responsive cytoprotective protein with diverse functions where one of its main roles have been attributed to oxidative stress protection.…”