GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE338nnn/GSE338973/primary200OKTranscriptomicsCaenorhabditis elegansExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE338973GEOGSEfalseFOXO/DAF-16 modulates the transcription factor ROR/NHR-23 and inhibits the let-7 microRNA to maintain multipotency during dauerAnimals rapidly reprogram gene expression to adapt development to environmental stress. How gene regulatory programs that drive continuous development are repressed during stress-induced developmental arrest remains poorly understood. In Caenorhabditis elegans, starvation and overcrowding trigger entry into the stress-resistant, quiescent dauer stage. Here, we identify interactions among the conserved transcription factors DAF-16/FOXO and NHR-23/ROR, and the let-7 family of microRNAs as key regulators of the switch from continuous development to dauer. We show that loss of daf-16 during dauer causes elevated let-7 family microRNAs and premature expression of the adult collagen reporter col-19p::GFP. Reducing let-7 family activity suppresses this phenotype, whereas dauer-specific let-7 expression is sufficient to induce col-19p::GFP expression. Mechanistically, DAF-16 inhibits let-7 transcription in part by repressing nhr-23, which encodes a transcriptional activator of the let-7 family and molting-cycle genes. ChIP-seq analysis reveals DAF-16 binding upstream of nhr-23, and daf-16; daf-7 mutant dauers exhibit increased nhr-23 mRNA and NHR-23 protein, supporting a model in which DAF-16 directly represses nhr-23. Integrated ChIP-seq and transcriptomic analyses identify 1,183 genes activated and 681 genes repressed by DAF-16 during dauer. Repressed targets are enriched for pro-growth genes involved in mitotic DNA replication and translational elongation. DAF-16 targets include 59 transcription factors that may mediate broader transcriptional reprogramming during dauer to maintain multipotency and establish quiescence. Together, these findings reveal that DAF-16/FOXO establishes stress-induced developmental arrest by coupling activation of protective pathways with repression of conserved developmental timing, growth, and differentiation programs.2026/07/17GSE338973GSM9885886GSM9885885GSM9885888GSM9885887GSM9885901GSM9885889GSM9885900GSM9885903GSM9885902GSM9885880GSM9885882GSM9885881GSM9885884GSM9885883GSM9885905GSM9885904GSM9885907GSM9885906GSM9885909GSM9885908GSM9885875GSM9885897GSM9885896GSM9885874GSM9885910GSM9885899GSM9885877GSM9885898GSM9885876GSM9885879GSM9885878GSM9885911GSM9885891GSM9885890GSM9885893GSM9885871GSM9885892GSM9885870GSM9885895GSM9885873GSM9885872GSM988589426672338973Caenorhabditis elegans[42538964]