Mutations in DJ-1 (also known as PARK7) are associated with inherited Parkinson disease and neuronal death, although the underlying molecular mechanisms have been unclear. Given that DJ-1 is highly conserved, Simon Møller and colleagues investigated the cellular function of an Arabidopsis thaliana homologue of DJ-1, AtDJ-1a (p. 1644). They first show that AtDJ-1a expression increases in response to many types of stress, including excessive light exposure and oxidative stress. In addition, aging AtDJ-1a-null (but not young) plants suffer larger and more-frequent lesions than wild-type plants following stress exposure. Closer investigation reveals that these lesions occur owing to increased plant-cell death resembling cell death that occurs in human neurons expressing mutant DJ-1. At-DJ-1a is found to interact with and increase the activity of the copper-dependent enzymes CSD1 and AtGPX2, which decrease cellular levels of damaging reactive oxygen species (ROS). Furthermore, DJ-1 interacts with the human homologues of these enzymes (SOD1 and GPX2, respectively). The authors propose that DJ-1 mediates a protective effect in stressed cells through delivering copper to antioxidant enzymes, thereby promoting their activity and reducing cell death resulting from excessive ROS levels.