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J. Biol. Chem., Vol. 282, Issue 2, 1144-1151, January 12, 2007

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Sequestration of Retinyl Esters Is Essential for Retinoid Signaling in the Zebrafish Embryo^*

Andrea Isken, Jochen Holzschuh¹, Johanna M. Lampert², Lara Fischer, Vitus Oberhauser, Krzysztof Palczewski^¶, and Johannes von Lintig³

From the Departments of Neurobiology, and Developmental Biology, Institute of Biology I, Albert-Ludwigs University of Freiburg, Hauptstrasse 1, D-79104 Freiburg, Germany and the ^¶Department of Pharmacology, Case Western Reserve School of Medicine, Cleveland, Ohio 44106-4965

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.

Received for publication, September 26, 2006 , and in revised form, November 9, 2006.

^* This work was supported in part by Grant Li956-2 from the German Research Council (DFG) and a grant from the Ministry of Science and Art, Baden-Württemberg (to J. v. L.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Supported by the Wissenschaftliche Gesellschaft Freiburg.

² Present address: Harvard University, 16 Divinity Ave., Cambridge, MA 02138.

³ To whom correspondence should be addressed. Tel.: 49-761-203-2539; Fax: 49-761-203-2921; E-mail: lintig{at}biologie.uni-freiburg.de.

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