The better an animal can react to stressful conditions the longer it can live and possibly reproduce. Stress response and lifespan are under the control of two pathways of the endocrine system: the insulin/IGF-1 signaling pathway and a steroid hormone-signaling pathway. Mutations that alter the expression or function of the components of these pathways increase stress tolerance and lifespan. In D. melanogaster, mutants that reduce signaling the steroid hormone ecdysone show an increase in stress tolerance and lifespan. Although ecdysone signaling is important for stress resistance and lifespan, the molecular mechanism responsible remains to be elucidated. My thesis research focused on the ecdysone-induced family of zinc finger transcription factors known as the Broad-Complex (BR-C) as a possible downstream target of ecdysone mediated stress resistance and lifespan. I examined the role of BR-C in stress resistance and longevity by measuring the survival under varying conditions of flies that have altered BR-C expression. BR-C expression was altered by one of three methods: a P-element insertion into the BR-C loci that causes the misexpression of BR-C transcripts, heatshock overexpression of BR-C transgenes, and reducing BR-C transcript levels by RNAi. The results from these experiments suggest a complex correlation between BR-C expression and stress response. Global overexpression or underexpression of BR-C suggests a positive correlation between BR-C expression levels and stress resistance. Misexpression of BR-C transcripts by P-element insertion into the BR-C loci indicates an inverse correlation between BR-C expression levels and stress resistance. My thesis research allows us to conclude that BR-C mediates stress resistance and may be the downstream target of ecdysone mediated stress resistance at the molecular level.