Abstract
In many organisms, environmental experiences early in development can result in gene expression changes that arc maintained into adulthood. The nematode Caenarhobditis elegans makes such an experience dependent decision to reach adulthood via development through a reproductive pathway or through a morphologically and physiologically distinct juvenile dauer diapause stage. Transcriptional profiling of adult animals that have passed through the two pathways has identified many genes with marked expression shifts in control and post-dauer animals (Hallet al. in prep). I identified the dod-23p::g(p fusion, which showed expression in the in ASI sensory neuron of control but not of post-dauer animals, as a marker gene tbr further study. I attempted to molecularly characterize the dauer-induced expression change of dod-23 in AS! by examining p;{p expression in mutant worms in different gene regulatory pathways (TGF-β, siRNA, miRNA, and chromatin remodeling) transgenic for a dod-23p::gfp fusion. Since dod- 23 and ASI head neurons are both implicated in C. elegans longevity, I also performed survival analyses of wild-type control and post-dauer worms, showing that post-dauer animals exhibit a significantly extended mean life span. To examine the regulatory mechanism resulting in post-dauer longevity, I performed survival analyses of mutant worms of the same pathways described above. First, the TGF-β pathway eliminated post-daucr effects in both gfp expression and longevity phenotype. Partial reduction of post-dauer efiects in gfp expression, longevity, or both were observed in the RNAi and chromatin remodeling pathways. My results show there is molecular memory of dauer-passagc that mediates animal longevity.