In transgenic tobacco plants containing a pea ferredoxin transcribed region (Fed-1) driven by the cauliflower mosaic virus 35S promoter (P35S), light acts at a post-transcriptional level to control the abundance of Fed-1 mRNA in green leaves. To determine whether the light signal for this response involves photosynthesis, we treated transgenic seedlings with or without 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU), an inhibitor of photosynthetic electron transport. DCMU prevented the normal light response by blocking reaccumulation of Fed-1 transcripts when dark-adapted green plants were returned to the light. In contrast, reaccumulation of light-harvesting complex B (Lhcb) transcripts was unaffected by DCMU treatment. Because Fed-1 light regulation requires translation, we also examined polyribosome profiles. We found that Fed-1 transcripts accumulated on polyribosomes in the light but were found primarily in non-polyribosomal fractions in dark-adapted plants or in illuminated plants exposed to lower than normal light intensity or treated with DCMU. Surprisingly, although Lhcb mRNA abundance was not affected by DCMU, its polyribosomal loading pattern was altered in much the same way as was that of Fed-1 mRNA. In contrast, DCMU had no effect on either the abundance or the polyribosome profiles of endogenous histone H1 or transgenic P35S::CAT transcripts. Thus, our results are consistent with the hypothesis that a process coupled to photosynthesis affects the polyribosome loading of a subset of cytoplasmic mRNAs.