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Fig. 3 | BMC Biology

Fig. 3

From: Mitochondrial unfolded protein response transcription factor ATFS-1 promotes longevity in a long-lived mitochondrial mutant through activation of stress response pathways

Fig. 3

Loss of ATFS-1 during development or adulthood alone is not sufficient to decrease nuo-6 longevity. a To explore the timing requirements for the role of ATFS-1 in nuo-6 longevity and the activation of the mitoUPR, nuo-6 worms were treated with RNAi against atfs-1 for development only (atfs-1 ➔ dcr-1), adulthood only (EV ➔ atfs-1) or for both development and adulthood (atfs-1atfs-1). Quantitative real-time RT-PCR was used to confirm knockdown of atfs-1, dcr-1 and the ATFS-1 target gene hsp-6. Treatment with dcr-1 RNAi during adulthood effectively decreased the expression of dcr-1 (b). The levels of atfs-1 mRNA were decreased by atfs-1 RNAi during adulthood only or development and adulthood (c). Transfer from atfs-1 RNAi to dcr-1 RNAi resulted in a restoration of atfs-1 mRNA levels towards EV control. Similarly, the levels of the atfs-1 target gene hsp-6 were decreased by atfs-1 RNAi during adulthood only or development and adulthood (d). Transfer from atfs-1 RNAi to dcr-1 RNAi resulted in a complete restoration of hsp-6 expression. e Knocking down atfs-1 levels only during adulthood does not affect nuo-6 lifespan. f Knocking down atfs-1 only during development does not significantly reduce nuo-6 lifespan. In contrast, atfs-1 RNAi applied during both development and adulthood decreased nuo-6 longevity. Error bars indicate SEM. **p < 0.01, ***p < 0.001. See Additional file 4: Table S4 for raw lifespan data. See Additional file 5: Table S5 for details on N and replicates

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