Fig. 5. PQM-1 activity regulates vitellogenin expression and lipid content of progeny in hypoxic stress.

a Quantification of matricide and embryonal stages in the uterus of hermaphrodites from ORO stained animals in (b). WT (N2) (n = 69) and pqm-1(ok485) (n = 77) in control condition; WT (N2) (n = 70) and pqm-1(ok485) (n = 65) in CoCl₂ condition; Chi-square analysis was performed; three independent experiments. b Oil Red O-based lipid staining displaying progeny in parental hermaphrodites. Parental hermaphrodites were Oil Red O stained at the day-1 of adulthood stage (control). CoCl₂ challenged hermaphrodites were exposed to 2.5 mM CoCl₂ at the day-1 of adulthood stage for 44 h followed by Oil Red O staining. Animals were synchronized at the L4 larval stage for adult analyses. Scale bars: 200 µm, in inset: 100 µm. c, d Lipid content of eggs (c) dissected from Oil Red O stained hermaphrodites challenged with 0.4% oxygen for 44 h and quantification of fat levels in eggs (d). WT (N2) eggs (n = 13) and pqm-1(ok485) eggs (n = 13) in control condition; WT (N2) eggs (n = 12) and pqm-1(ok485) eggs (n = 12) in hypoxic condition; scale bars: 25 µm. Two-tailed t-test, Two-way ANOVA (✝), mean ± SD, three independent experiments. e, f pqm-1- and CoCl₂-dependent regulation of endogenous vitellogenins determined by RT-qPCR (n = 3 biological replicates) for control condition (e) and condition of 5 mM CoCl₂ exposure (f). Reduction of vit gene expression in pqm-1 mutants relative to WT is indicated below the p-value and the corresponding fold change value is displayed in brackets (e). Quantification values were normalized to mean value of WT control without CoCl₂ (e, f). Animals were exposed to 5 mM CoCl₂ for 6 h at early adulthood. Two-tailed t-test (e, f), mean ± SD, ns = not significant.