Data from: Complex I superoxide anion production is necessary and sufficient for Complex I inhibitor-induced dopaminergic neurodegeneration in Caenorhabditis elegans

Inhibitors of electron transport chain Complex I (CI) have long been associated with and are now used to model Parkinson's disease (PD), but CI inhibition results in multiple effects including ATP depletion and reactive oxygen species (ROS) generation. The lack of tools to isolate effects of CI inhibition have rendered it difficult to determine which mechanistic step is critical for CI inhibitor-induced dopaminergic neurodegeneration. Here we report that CI-derived superoxide anion, not ATP depletion, is the critical driver of CI inhibitor-induced dopaminergic neurodegeneration in the model organism Caenorhabditis elegans. We first use SuperNova, a light-activated ROS-generating protein, fused to CI to demonstrate that in absence of enzymatic inhibition CI-localized ROS production is sufficient to drive morphological damage and loss of function of the dopaminergic neurons. Second, we prevented superoxide anion production during exposure to the CI inhibitors rotenone and pyridaben and report a full rescue of CI inhibitor-induced degeneration and functional loss, without rescue of inhibitor-induced ATP depletion.
This dataset includes data files recording worm length after stressor exposure; neuronal damage scoring after exposure; dopaminergic redox and bioenergetics states after exposure; and a data dictionary.