Thyroid hormone-induced swim bladder and eye maturation are transduced by IGF-1 in zebrafish embryos

Abstract

Maternally derived thyroid hormones (THs) deposited in yolk promote fish embryogenesis and survival, and understanding early regulatory mechanisms could lead to improved seedstock production. We have tested the hypothesis that some thyroid actions may be mediated by insulin-like growth factor I (IGF-1), another promoter of embryo development. Differentiation and performance were assessed in embryos treated with THs in the presence or absence of an IGF-1 receptor blocking peptide. Treatment with the TH triiodothyronine (T3) promoted IGF-1 gene expression at days 1 and 5, and advanced swim bladder and eye development, but blocking the IGF-1 receptor eliminated the swim bladder and eye effects. Growth and survival at 1 week of age were impaired by the IGF-1 receptor blocking peptide alone, but concurrent treatment with T3 partially restored these indices. Our results confirm interaction of T3 and IGF-1 regulatory signalling in zebrafish embryogenesis and transduction by IGF-1 of thyroid-driven swim bladder and eye maturation.