Marine diatoms are known to be responsible for about a quarter of global primary production and their photosynthesis is sustained by inorganic carbon-concentrating mechanisms and/or C(4) metabolism. Activities of the inorganic carbon-concentrating mechanism are attenuated under enriched [CO(2)]; however, impacts of this factor on primary productivity and the molecular mechanisms of CO(2) responses in marine diatoms are unknown. In this study, transgenic cells were generated of the marine diatom Phaeodactylum tricornutum by the introduction of a beta-glucuronidase reporter gene under the control of an intrinsic CO(2)-responsive promoter, which is the sequence between -80 to +61 relative to the transcription start site of a chloroplastic-carbonic anhydrase gene, ptca1, obtained from P. tricornutum. The activity of the ptca1 promoter was effectively repressed in air-level CO(2) by treating cells with a 1.0 mm cAMP analog, dibutyryl cAMP, or a cAMP phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine. Deletion of the intrinsic cAMP-response element from the ptca1 promoter caused a lack of repression of the reporter gene uidA, even under elevated [CO(2)] and a null phenotype to the strong repressive effects of dibutyryl cAMP and 3-isobutyl-1-methylxanthine on the ptca1 promoter. Deletion of the cAMP-response element was also shown to cause derepression of the uidA reporter gene in the dark. These results indicate that the cytosolic cAMP level increases under elevated [CO(2)] and represses the ptca1 promoter. This strongly suggests the participation of cAMP metabolism, presumably at the cytosolic level, in controlling CO(2)-acquisition systems under elevated [CO(2)] at the ocean surface in a marine diatom.