Research Paper Volume 8, Issue 9 pp 1979—2005

An intestinal microRNA modulates the homeostatic adaptation to chronic oxidative stress in C. elegans

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Figure 5. The mir-60 loss-induced enhanced resistance against the long-term mild oxidative stress is significantly suppressed by RNAi inactivations against target candidates. (A) Survival curves of wild-type and mir-60 mutant animals treated with each RNAi are shown. ‘EV’ denotes Empty Vector control in feeding RNAi. Small bar graphs indicate the percentage of RNAi-induced lifespan reduction compared to the EV control for each strain. All these lifespan assays were performed at 20 °C under the PQ 5 mM condition. Error bars represent SE calculated from 3-4 replicates. The detailed results are available in Supplemental Fig 3B. (B) Mature miR-60 strand (miR-60-3p) and its possible binding sites in 3' UTR of target candidates are shown by vertical lines. Sequence alignments are based on TargetScan and RNAhybrid programs [46,88]. Conserved regions among C. elegans (cel)-related species, including C. briggsae (cbr), C. remanei (crm), C. brenneri (cbn) and C. japonia (cjp), are highlighted by while-colored letters on gray backgrounds. Additional results are shown in Supplemental Fig 3C.