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. 2023 Apr 12;616(7958):814–821. doi: 10.1038/s41586-023-05922-y

Extended Data Fig. 8. Physiological consequences of reducing Pol-II elongation speed in animal models.

Extended Data Fig. 8

(a) Survival of wild-type and ama-1(m322) mutant worms conferring a slow Pol-II elongation rate (4 replicates, BR1:1.267, P < 0,0001; BR2:1.23,P < 0.0001; BR3:1, P = 0.0342; BR4:1.263,P < 0.0001, log-rank test, Mantel-cox). (b) C. elegans lifespan analysis after CRISPR/Cas9 mediated reversion of the slow RNAPII mutation. Survival curves of the strain harbouring the slow RNAPII mutation (ama-1 m322) and wild-type controls compared to worms after CRISPR/Cas9 engineered reversion of the slow mutation back to the wild type allele (ama-1 syb2315). Animals with slow Pol-II have a significantly increased lifespan. CRISPR/Cas9 engineered reversion restored lifespan essentially back to wild-type levels. (3 replicates; n > 300 per strain). (c) Pumping rates of wild type N2 (day 1: 47 worms, day 8: 49 worms) and ama-1 mutant (day 1: 52 worms, day 8: 48 worms) worms were measured on day 1 and day 8. Pumping rates were not significantly different on day 1, but ama-1 worms showed higher pumping rates compared to wild types on day 8, suggesting that the mutant worms are healthier at old age. The error bars represent standard deviation. (d) Ex-vivo S35 incorporation assay shows no significant difference in translation rates in female fly heads between wDah control and RpII215C4 mutants both at young (10days) and old age (50 days). N = 5 biological replicates with 25 heads per replicate. The error bars show the standard error of the mean.