Sequestration of retinyl esters is essential for retinoid signaling in the zebrafish embryo.

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Isken A, Holzschuh J, Lampert JM, Fischer L, Oberhauser V, Palczewski K, von Lintig J

Sequestration of retinyl esters is essential for retinoid signaling in the zebrafish embryo.

J Biol Chem. 2007 Jan 12;282(2):1144-51. Epub 2006 Nov 10.

PubMed ID

17098734 [ View in PubMed

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Abstract

For vertebrate development, vitamin A (all-trans retinol) is required in quantitative different amounts and spatiotemporal distribution for the production of retinoic acid, a nuclear hormone receptor ligand, and 11-cis retinal, the chromophore of visual pigments. We show here for zebrafish that embryonic retinoid homeostasis essentially depends on the activity of a leci-thin:retinol acyltransferase (Lratb). During embryogenesis, lratb is expressed in mostly non-overlapping domains opposite to retinal dehydrogenase 2 (raldh2), the key enzyme for retinoic acid synthesis. Blocking retinyl ester formation by a targeted knock down of Lratb results in significantly increased retinoic acid levels, which lead to severe embryonic patterning defects. Thus, we provide evidence that a balanced competition between Lratb and Raldh2 for yolk vitamin A defines embryonic compartments either for retinyl ester or retinoic acid synthesis. This homeostatic mechanism dynamically adjusts embryonic retinoic acid levels for gene regulation, concomitantly sequestering excess yolk vitamin A in the form of retinyl esters for the establishment of larval vision later during development.

DrugBank Data that Cites this Article

Drug Targets

Drug	Target	Kind	Organism	Pharmacological Action	Actions
Vitamin A	Retinal dehydrogenase 2	Protein	Humans	Unknown	Substrate	Details