Intense and excessive light triggers the evolution of reactive oxygen species in chloroplasts, and these have the potential to cause damage. However, plants are able to respond to light stress and protect the chloroplasts by various means, including transcriptional regulation at the nucleus. Activation of light stress–responsive genes is mediated via hydrogen peroxide–dependent and –independent pathways. In this study, we characterized the Early-Light–Inducible Protein 2 (ELIP2) promoter–luciferase gene fusion (ELIP2::LUC), which responds only to the hydrogen peroxide–independent pathway. Our results show that ELIP2::LUC is expressed under nonstressful conditions in green tissue containing juvenile and developing chloroplasts. Upon light stress, expression was activated in leaves with mature as well as developing chloroplasts. In contrast to another high-light–inducible gene, APX2, which responds to the hydrogen peroxide–dependent pathway, the activation of ELIP2::LUC was cell autonomous. The activation was suppressed by application of 3-(3,4)-dichlorophenyl-1,1-dimethylurea, an inhibitor of the reduction of plastoquinone, whereas 2,5-dibromo-3-methyl-6-isopropyl-p-benzoquinone, an inhibitor of the oxidation of plastoquinone, gave the contrasting effect, which may suggest that the redox state of the plastoquinone plays an important role in triggering the hydrogen peroxide–independent light stress signaling.