Figure 2. Analysis of retinoic acid as a transcription factor or retinoid analog. A: Relative expression of ultraviolet (UV)-cone opsin messenger RNA (mRNA) in retinal pigment epithelium-specific protein 65kDa and rhodopsin (Rpe65^−/− Rho^−/−) explants. Explants were treated with 11-cis retinal, 11-cis retinol, retinoic acid (RA), retinoic acid receptor (RAR)-agonist and retinoid X-receptor (RXR)-agonist, respectively. An equal amount of messenger RNA (mRNA) was used from each group for quantitative RT-PCR and normalized to β-actin. All compounds increased UV–cone opsin mRNA expression (*p<0.01; **p<0.001; ***p<0.0001). B: Transducin activation by the mouse UV cone opsin in the absence and presence of 11-cis retinal and all-trans retinoic acid (RA) was examined. Activity has been corrected for intrinsic transducin activity in the absence of opsin and ligand using mock-transfected green monkey kidney cell (COS-1) membranes. RA was also added to the mock-transfected COS-1 cell membranes to ensure any ligand had no effect on endogenous COS-1 cell proteins. The RA concentrations used were 20 and 200 µM. As expected, 11-cis retinal was found to act as an inverse agonist for mouse UV–cone opsin; RA was found to act as an agonist for UV–cone opsin, increasing transducin activity using either one of the two concentrations.