Mitochondrial and metabolic perturbations result in numerous alterations in gene expression. The Haynes Lab focuses on the mitochondrial UPR, an intra-cellular stress response that modulates gene expression to repair and recover mitochondrial activity. We have uncovered a novel form of transcriptional regulation based on organelle partitioning of a single transcription factor (ATFS-1 in worms, ATF5 in mammals) that allows cells to evaluate mitochondrial function or dysfunction and adjust transcription accordingly. Researchers in the laboratory examine how ATFS-1 is further regulated and integrates with other metabolic stress response pathways to promote survival during mitochondrial dysfunction.