Effect of depletion of NHR-114/HNF4, and maternal B12 treatment on gene expression of C. elegans in Larva 4 stage.

Vitamin B12 (B12) deficiency is a critical problem worldwide. Such deficiency in infants has long been known to increase the propensity to develop obesity and diabetes later in life through unclear mechanisms. Here, we establish a ∆nhr-114 animal as a Caenorhabditis elegans model to study how early-life B12 impacts adult health. We find that early-life B12 deficiency causes increased lipogenesis and lipid peroxidation in adult worms, which in turn induces germline defects through ferroptosis. In order to further identify genes that respond to early-life B12, we carried out an RNA sequencing (RNA-seq) assay to analyze the gene expression profiles of WT and ∆nhr-114 animals maternally supplied with 8 μM B12 or not. Comparative gene expression profiling analysis of RNA-seq data for WT, ∆nhr-114 animals (Larva 4 stage) with or without maternal B12 treatment (8 μM).