Kiefer Cornelia, Sumser Emerich, Wernet Mathias F, Von Lintig Johannes
Institute of Biology I, Neurobiology, and Animal Physiology, Albert-Ludwig University of Freiburg, Hauptstrasse 1, D-79104 Freiburg, Germany.
Proc Natl Acad Sci U S A. 2002 Aug 6;99(16):10581-6. doi: 10.1073/pnas.162182899. Epub 2002 Jul 22.
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.
目前，类胡萝卜素降低慢性病风险和维生素A缺乏风险的潜力正受到深入研究。在维生素A缺乏并非致命的无脊椎动物模型中，可以分离出在从膳食类胡萝卜素到维生素A的途径中受影响的失明但存活的突变体。利用其中一个模型系统（果蝇）中的一个突变体，最近已从分子水平鉴定出维生素A形成酶。我们现在表明，另一个果蝇突变体ninaD失明的分子基础是类胡萝卜素细胞摄取缺陷。ninaD基因编码一种对视觉发色团形成至关重要的B类清道夫受体。该功能丧失会导致无类胡萝卜素，从而出现维生素A缺乏的表型。我们的研究提供了关于类胡萝卜素如何分布到动物靶组织细胞中的分子见解，并表明B类清道夫受体在使膳食类胡萝卜素可用于后续细胞代谢方面起着关键作用，这是其各种生理功能所必需的。
