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Retinyl ester formation by lecithin:retinol acyltransferase (LRAT) is a key regulator of retinoid homeostasis in mouse embryogenesis
Author(s) -
Wassef Lesley,
Kim YounKyung,
Hamberger Leora,
Palczewski Krzysztof,
Blaner William S,
Quadro Loredana
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.313.7
Subject(s) - retinoid , retinol , retinoic acid , acyltransferase , embryogenesis , endocrinology , biology , vitamin , retinyl palmitate , medicine , embryo , vitamin a deficiency , microbiology and biotechnology , chemistry , biochemistry , enzyme , gene
The developing mammalian embryo is entirely dependent on the maternal circulation for its supply of retinoids (vitamin A and its derivatives). The mechanisms through which mammalian developing tissues maintain adequate retinoid levels in the face of perturbations in maternal vitamin A dietary intake have not been established. We investigated the role of retinyl ester formation catalyzed by lecithin:retinol acyltransferase (LRAT) in regulating retinoid homeostasis during embryogenesis. Pregnant mice, lacking both LRAT and retinol‐binding protein (RBP), the serum specific carrier for retinol, were maintained on diets containing different amounts of vitamin A. Maternal dietary vitamin A deprivation during pregnancy generated a severe retinoid‐deficient phenotype of the embryo due to the retinoid deficient status of the double mutant dams rather than to the lack of embryonic LRAT. Moreover, LRAT acts together with Cyp26A1, one of the enzymes that catalyze the degradation of retinoic acid, and possibly with Stra6, the recently identified cell surface receptor for retinol‐RBP, in maintaining adequate levels of retinoids in embryonic and extraembryonic tissues. Work supported by the National Research Initiative Grant no. 2006‐35200‐16580 from the USDA‐CSREES, Program 31.0.