Transcription profiling of C. elegans wildtype and gas-1 mitochondrial mutants

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 hypomorhpic C. elegans mutants in nuclear-encoded subunits of respiratory chain complexes I, II and III. Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Experiment Overall Design: 5 biological replicates of wildtype and electron transport chain (ETC) mutant C. elegans were used as sources of total RNA, each for hybridization to a single Affymetrix whole-genome microarray. Comparison of the data was intended to reveal metabolic pathways downstream of the mutation.