Light regulates the development of Arabidopsis seedlings in a variety of ways, including inhibition of hypocotyl growth and promotion of leaf development, chloroplast differentiation, and light-responsive gene expression. Mutations that uncouple most or all of these responses from light control have been described, for example, det1, det2, and cop1. To identify regulatory components that define downstream branches in the light-regulated signal transduction pathway, mutants specifically affected in only one light-regulated response were isolated. A screen was designed to isolate mutants that overexpressed the CAB (photosystem II type I chlorophyll a/b-binding proteins) genes in the dark, by use of transgenic line containing a T-DNA construct with two CAB3 promoter-reporter fusions. Eight mutants that showed aberrant expression of both CAB3 promoters were isolated and were designated doc mutants (for dark overepression of CAB). All of the mutants have normal etiolated morphology in the dark. Genetic and phenotypic analyses indicate that most of the mutations are recessive and define at least three loci (doc1, doc2, doc3). Unlike det1 and det2 mutants, which affect the expression of CAB and RBCS (the small subunit of RuBP carboxylase) to approximately the same extent, all three doc mutations are much more specific in derepressing the expression of CAB. The phenotypes of doc mutants suggest that morphological changes can be genetically separated from changes in CAB gene expression. Moreover, the regulation of CAB gene expression can be separated further from the regulation of RBCS gene expression. Epistasis studies suggest that DOC1 and DET3 act downstream from DET1 on two separate branches in the phototransduction pathway. In contrast, DOC2 appears to act on a distinct pathway from DET1. Mutations in doc1, doc2, or doc3 also impair plant growth under short-day conditions.