Fig. 4: HIF-1 targets required for adaptive survival.
From: The hypoxia response pathway promotes PEP carboxykinase and gluconeogenesis in C. elegans
a Heatmap of row Z-scores for qRT-PCR measurements from L4-stage animals of transcript levels for the indicated genes (rows) as normalized to actin. Columns indicate the genotypes (either wild type or hif-1(ia4) mutants) and experimental conditions (4 h under either normoxia or hypoxia (0.5% O2), with four replicates from each genotype/condition shown. b, d Percent of L4-stage animals, grown on fixed E. coli, to survive liquid culture without food and under hypoxia (0.5% O2, 48 h at 25 °C, with 24 h recovery at 20 °C). Error bars indicate mean ± SEM. c, e Percent of embryos, obtained from animals grown on fixed E. coli, to survive 24 h of hypoxia at 25 °C, with 24 h recovery at 20 °C. Animals are indicated by colored symbols, and associated figure legends list the condition in which they were grown: on plates supplemented with either metabolites or antioxidants. Error bars indicate mean ± SEM. For graphs (b–e), ****P < 0.0001, ***P < 0.001, **P < 0.01, *P < 0.05 ANOVA/Sidak’s multiple comparison two-sided test between each supplement and the no-supplement control. #P < 0.0001 ANOVA/Sidak’s multiple comparison two-sided test between the indicated mutant versus wild-type, both no-supplement controls. Data for each column in (b, c) represents four biological replicates, and in (d, e) represents six biological replicates, typically 20–100 animals per replicate. f Model illustrating how HIF-1 binds near the pck-1 promoter to upregulate PCK-1 expression and drive gluconeogenesis and the production of antioxidants.
