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. 2014 Oct 30;3(3):e959404. doi: 10.4161/21624046.2014.959404

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Figure 1. — Mitochondrial dysfunction induces the UPR^mt in a cell autonomous and non-autonomous fashion, but does not require the UPR^mt for longevity. The C. elegans UPR^mt can be monitored by the transcriptional upregulation of mitochondrial chaperone genes including hsp-6 and hsp-60. Electron transport chain inhibition by RNAi knockdown of cco-1 (indicated by lightning bolts) in neurons or the intestine is sufficient for lifespan extension in worms and causes obvious induction of the hsp-6_p::gfp reporter in intestinal cells (Panels 1 and 2). Loss of function in the UPR^mt transcription factor atfs-1 prevents induction of hsp-6_p::gfp following cco-1(RNAi) but does not prevent lifespan extension (Panel 3).