Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorphic C. ele; Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Experiment Overall Design: 3 biological replicates of each C. elegans strain were used as sources of total RNA combined for hybridization to a single Affymetrix whole-genome microarray. Comparison of the data was intended to reveal metabolic pathways downstream of the mutation.