期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 99, 期 16, 页码 10581-10586出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.162182899
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Carotenoids are currently being intensely investigated regarding their potential to lower the risk of chronic disease and vitamin A deficiency. Invertebrate models in which vitamin A deficiency is not lethal allow the isolation of blind but viable mutants affected in the pathway leading from dietary carotenoids to vitamin A. Using a mutant in one of these model systems, Drosophila, the vitamin A-forming enzyme has recently been molecularly identified. We now show that the molecular basis for the blindness of a different Drosophila mutant, ninaD, is a defect in the cellular uptake of carotenoids. The ninaD gene encodes a class B scavenger receptor essential for the formation of the visual chromophore. A loss of this function results in a carotenoid-free and thus vitamin A-deficient phenotype. Our investigations provide molecular insight into how carotenoids may be distributed into cells of target tissues in animals and indicate a crucial role of class B scavenger receptors rendering dietary carotenoids available for subsequent cell metabolism, as needed for their various physiological functions.
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