First Author | Pessôa CN | Year | 2008 |
Journal | Invest Ophthalmol Vis Sci | Volume | 49 |
Issue | 5 | Pages | 2039-45 |
PubMed ID | 18436838 | Mgi Jnum | J:135203 |
Mgi Id | MGI:3790586 | Doi | 10.1167/iovs.07-0908 |
Citation | Pessoa CN, et al. (2008) Thyroid hormone action is required for normal cone opsin expression during mouse retinal development. Invest Ophthalmol Vis Sci 49(5):2039-45 |
abstractText | PURPOSE: The expression of S- and M-opsins in the murine retina is altered in different transgenic mouse models with mutations in the thyroid hormone receptor (TR)-beta gene, demonstrating an important role of thyroid hormone (TH) in retinal development. METHODS: The spatial expression of S- and M-opsin was compared in congenital hypothyroidism and in two different TR mutant mouse models. One mouse model contains a ligand-binding mutation that abolishes TH binding and results in constitutive binding to nuclear corepressors. The second model contains a mutation that blocks binding of coactivators to the AF-2 domain without affecting TH binding. RESULTS: Hypothyroid newborn mice showed an increase in S-opsin expression that was completely independent of the genotype. Concerning M-opsin expression, hypothyroidism caused a significant decrease (P < 0.01) only in wild-type animals. When TRbeta1 and -beta2 were T3-binding defective, the pattern of opsin expression was similar to TRbeta ablation, showing increased S-opsin expression in the dorsal retina and no expression of M-opsin in the entire retina. In an unexpected finding, immunostaining for both opsins was detected when both subtypes of TRbeta were mutated in the helix 12 AF-2 domain. CONCLUSIONS: The results show, for the first time, that the expression of S- and M-opsin is dependent on normal thyroid hormone levels during development. |