PUBLICATION
Sequestration of retinyl esters is essential for retinoid signaling in the zebrafish embryo
- Authors
- Isken, A., Holzschuh, J., Lampert, J.M., Fischer, L., Oberhauser, V., Palczewski, K., and von Lintig, J.
- ID
- ZDB-PUB-061116-13
- Date
- 2007
- Source
- The Journal of biological chemistry 282(2): 1144-1151 (Journal)
- Registered Authors
- Holzschuh, Jochen, Lampert, Johanna
- Keywords
- none
- MeSH Terms
-
- Retinoids/metabolism*
- Cell Line
- Drosophila
- Tretinoin/metabolism
- Aldehyde Oxidoreductases/genetics
- PubMed
- 17098734 Full text @ J. Biol. Chem.
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 lecithin: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 a significant 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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping