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Increasing evidence suggests that deficits in mitochondrial function, oxidative and nitrosative stress, accumulation of aberrant or misfolded proteins, and ubiquitin-proteasome system dysfunction may represent the principal molecular pathways that commonly underlie the pathogenesis of neurodegenerative Parkinson’s disease (PD). Mutations in human DJ-1 lead to early onset PD. The subcellular distribution of DJ-1 (PARK7) is primarily cytoplasmic with smaller quantities found associated with mitochondria. Postulated functions include roles in the oxidative stress response, either as a redox sensor protein that can prevent the aggregation of alpha-synuclein or as an antioxidant. Homologs of DJ-1 are found in all kingdoms of life. To understand the functions of plant DJ-1 homologs we identified null mutants in the model plant Arabidopsis thaliana. One of the 3 Arabidopsis genes encoding DJ1 homologs (DJ1C) is essential for viability, and null knockout mutants are seedling lethal.