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. 2023 Jan 16;14:240. doi: 10.1038/s41467-023-35899-1

Fig. 3. Alpha-KB promotes peroxisome function and biogenesis via the NAD+-SIR-2.1 pathway.

Fig. 3

a Representative images of peroxisomes in glp-1(e2141ts) mutant worms expressing vha-6p::mRFP-PTS1. Scale bars: 2.5 μm. Veh vehicle. b The number of peroxisomes was increased in glp-1(e2141ts) mutants. RNAi knockdown of either cth-1 or cth-2 inhibited this increase, which was rescued by supplementation with α-ketobutyrate (α-KB, 500 μM). Data were presented as mean values ± SEM of three independent experiments (n = 25 worms per experiment). c Representative images of peroxisomes in transgenic worms expressing vha-6p::mRFP-PTS1 after treatment with α-KB. d Supplementation with α-KB (500 μM) increased the number of peroxisomes in worms, which was inhibited by RNAi knockdown of either ldh-1 or sir-2.1. Data were presented as mean values ± SEM of three independent experiments (n = 25 worms per experiment). e Representative images of acox-1.2p::gfp in glp-1(e2141ts) worms. Scale bars: 150 μm. f Expression of acox-1.2p::gfp was upregulated in glp-1(e2141ts) mutants. RNAi knockdown of either cth-1 or cth-2 inhibited this increase, which was rescued by supplementation with α-KB (500 μM). Data were presented as mean values ± SEM of three independent experiments (n = 35 worms per experiment). g Representative images of acox-1.2p::gfp in worms after treatment with α-KB. h Supplementation with α-KB (500 μM) increased the expression of acox-1.2p::gfp in WT worms, which was inhibited by RNAi knockdown of either ldh-1 or sir-2.1. Data were presented as mean values ± SEM of three independent experiments (n = 35 worms per experiment). P values throughout were calculated using a one-way ANOVA followed by a Student–Newman–Keuls test. Source data are provided as a Source Data file.