GSE107784
mitoCPR  - a surveillance pathway that protects mitochondria in response to mitochondrial import stress
Mitochondrial functions are essential for cell viability and rely on protein import into the organelle. Various disease and stress conditions can lead to mitochondrial import defects. We find that inhibition of mitochondrial import in budding yeast activates a surveillance mechanism, mitoCPR, that is aimed at ameliorating mitochondrial import and protecting mitochondria during import stress. mitoCPR induces expression of Cis1 which associates with the mitochondrial translocase to reduce the accumulation of mitochondrial precursor proteins at the organelle surface. Clearance of precursor proteins depends on the Cis1 interacting AAA+ ATPase Msp1 and the proteasome suggesting that Cis1 facilitates degradation of un-imported proteins at the mitochondrial surface. Overall design: Five replicates of Empty Vector controls, six replicates of PSD1 overexpressors, six replicates of  PSD1 overexpressors harboring a PDR3 deletion and five replicates of V5-PSD1 overexpressors.