A class B scavenger receptor mediates the cellular uptake of carotenoids in <i>Drosophila</i>

TLDR

Carotenoids are studied for their potential to reduce chronic disease risk and prevent vitamin A deficiency, and invertebrate models enable investigation of the pathway from dietary carotenoids to vitamin A. The ninaD gene encodes a class B scavenger receptor required for cellular uptake of carotenoids; loss of ninaD causes a carotenoid‑free, vitamin‑A‑deficient phenotype, revealing that class B scavenger receptors are crucial for delivering dietary carotenoids to target tissues.

Abstract

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.