We are interested in understanding the interplay between chromatin dynamics, gene expression regulation, stress response, and aging. We use C. elegans as a model to dissect how specific chromatin factors influence stress response and longevity, and explore how global chromatin and gene expression dynamics change under stress and during aging. Recently, we demonstrated that the chromatin factors SET-26 and HCF-1 act in the soma to modulate stress response and longevity. We revealed that SET-26 localizes to chromatin by binding to the histone mark H3K4me3, subsequently recruiting HCF-1. Additionally, we identified the histone deacetylase HDA-1 playing an antagonizing role to SET-26/HCF-1. Interestingly, HDA-1 localizes to genomic regions closely aligned with the SET-26 and HCF-1 binding sites but is recruited to the chromatin independently of SET-26 or HCF-1. Gene expression profiling unveiled that SET-26/HCF-1 and HDA-1 exert opposing effects on the expression of specific target genes, which likely contribute to their antagonistic roles in longevity. In a parallel study, we explored how chromatin dynamics and gene expression changes contribute to the beneficial effects of hormesis. Hormesis, where prior exposure to mild stress enhances resilience to subsequent stress challenges, has been widely observed across species. We have established a robust experimental regimen in which C. elegans were "primed" by brief exposure to mild heat stress, followed by recovery and subsequent exposure to a lethal heat shock challenge. Primed worms consistently exhibited heightened resistance to subsequent heat shock, with improved survival and motility compared to naive worms. To investigate the potential gene regulatory mechanisms underlying these priming-induced protective effects, we conducted ATAC-seq and RNA-seq at several key time points. Our analyses revealed that both mild heat stress priming and subsequent heat shock challenge induced significant alterations in chromatin accessibility and RNA expression. Interestingly, the changes induced by priming were largely distinct from those induced by heat shock alone, suggesting that different levels of heat stress elicit distinct molecular responses. These genomic studies, coupled with functional analyses, led to the discovery of several new mediators of the protective effects of hormesis.