The role of the Arabidopsis transcription factor LONG HYPOCOTYL 5 (HY5) in promoting photomorphogenic development has been extensively characterized. Although the current model for HY5 action largely explains its role in this process, it does not adequately address the root phenotype observed in hy5 mutants. In our search for common mechanisms underlying all hy5 traits, we found that they are partly the result of an altered balance of signaling through the plant hormones auxin and cytokinin. hy5 mutants are resistant to cytokinin application, and double mutant analyses indicate that a decrease in auxin signaling moderates hy5 phenotypes. Microarray analyses and semiquantitative RT-PCR indicate that two negative regulators of auxin signaling, AUXIN RESISTANT 2 (AXR2)/INDOLE ACETIC ACID 7 (IAA7) and SOLITARY ROOT (SLR)/IAA14, are underexpressed in hy5 mutants. The promoters of these genes contain a putative HY5 binding site, and in line with this observation, HY5 can bind to the promoter of AXR2 in vitro. Increased AXR2 expression in a hy5 background partially rescues the elongated hypocotyl phenotype. In summary, it appears that auxin signaling is elevated in hy5 mutants because HY5 promotes the expression of negative regulators of auxin signaling, thereby linking hormone and light signaling pathways.