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ZFIN ID: ZDB-PUB-160124-2
Deiodinase knockdown affects zebrafish eye development at the level of gene expression, morphology and function
Houbrechts, A.M., Vergauwen, L., Bagci, E., Van Houcke, J., Heijlen, M., Kulemeka, B., Hyde, D.R., Knapen, D., Darras, V.M.
Date: 2016
Source: Molecular and Cellular Endocrinology   424: 81-93 (Journal)
Registered Authors: Bagci, Enise, Darras, Veerle, Hyde, David R., Knapen, Dries, Vergauwen, Lucia
Keywords: deiodinase, development, morpholino knockdown, retina, thyroid hormone, zebrafish
MeSH Terms:
  • Animals
  • Eye Abnormalities/etiology*
  • Gene Expression Profiling
  • Gene Expression Regulation, Developmental*
  • Gene Knockdown Techniques
  • Iodide Peroxidase/genetics*
  • Iodide Peroxidase/metabolism
  • Organ Size
  • Vision, Ocular
  • Zebrafish/genetics
  • Zebrafish/growth & development*
  • Zebrafish/metabolism
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed: 26802877 Full text @ Mol. Cell. Endocrinol.
Retinal development in vertebrates relies extensively on thyroid hormones. Their local availability is tightly controlled by several regulators, including deiodinases (Ds). Here we used morpholino technology to explore the roles of Ds during eye development in zebrafish. Transcriptome analysis at 3 days post fertilization (dpf) revealed a pronounced effect of knockdown of both T4-activating Ds (D1D2MO) or knockdown of T3-inactivating D3 (D3bMO) on phototransduction and retinoid recycling. This was accompanied by morphological defects (studied from 1 to 7 dpf) including reduced eye size, disturbed retinal lamination and strong reduction in rods and all four cone types. Defects were more prominent and persistent in D3-deficient fish. Finally, D3-deficient zebrafish larvae had disrupted visual function at 4 dpf and were less sensitive to a light stimulus at 5 dpf. These data demonstrate the importance of TH-activating and -inactivating Ds for correct zebrafish eye development, and point to D3b as a central player.