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Thyroid Hormone Action Is Required for Normal Cone Opsin Expression during Mouse Retinal Development

¹From the Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, CCS, Cidade Universitária, Ilha do Fundão, Rio de Janeiro, Brazil; the ²Metabolism Division, Departments of Pediatrics and Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland; and ³Laboratório Psicologia Experimental, USP, São Paulo, Brazil.

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)-β 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 TRβ1 and -β2 were T3-binding defective, the pattern of opsin expression was similar to TRβ 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 TRβ 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.