(27cc) Bacterial Metabolites Required for Post-Embryonic Development in C. Elegans

Nutrition intake influences animal growth, reproductive capacity, and survival of animals. Under poor nutritional conditions, animal development arrests as an adaptive survival strategy. Although development arrest is well recognized, the nutritional basis and the underlying nutrient-sensing mechanism essential for surpassing animal developmental arrest remain to be explored. In Caenorhabditis elegans, we observed developmental arrest in C. elegans when feeding on Lactobacillus plantarum and the rescue of the diapause state with trace supplementation of Escherichia coli. To identify the nutrition basis for the developmental arrest rescue, we performed a genome-wide screen using 3983 individual gene deletion E. coli mutants and identified 29 E. coli genes indispensable for initiating L1 larval growth that enables C. elegans development on L. plantarum. Among these crucial genes, we confirmed E. coli pdxH, and the downstream metabolite pyridoxal 5-P (PLP, Vitamin B6) as an essential nutritional factor for C. elegans postembryonic development. Transcriptome study on C. elegans revealed the regulatory function of pdxH relies on PLP-binding activity. Additionally, the bacterial PLP may act as a cofactor for host tyrosine aminotransferase, thereby promoting the translocation of daf-16 to the nucleus. Altogether, these results demonstrate that E. coli works with C. elegans in the biosynthesis of PLP, highlighting the role of microbial metabolite PLP to initiate postembryonic development in C. elegans.