title: The basis for colorless hemolymph and cocoons in the Y-gene recessive Bombyx mori mutants: a defect in the cellular uptake of carotenoids.
abstract: Bombyx mori is an excellent model for the study of carotenoid-binding proteins (CBP). In previous papers, we identified and molecularly characterized a CBP from the Y-gene dominant mutants. In the present study, we attempted to correlate and establish lipid metabolism and distribution in these mutants. When [3H]-triolein was fed to the mutants, typical patterns of uptake of labeled fatty acids from midgut to hemolymph and subsequent delivery to fat body and silk glands were obtained in all mutants. Further analysis of lipid and carotenoid profiles revealed that the yellow coloration in the hemolymph associated with lipophorin is not attributed to a difference in lipophorin concentrations among the mutants, nor to its lipid composition, but rather to its carotenoid content. Lipophorin of the Y+I mutant exhibited the highest concentration of total carotenoids of 55.8 microg/mg lipophorin compared to 3.1 microg/mg in the +Y+I mutant, 1.2 microg/mg in the YI mutant and 0.5 microg/mg in the +YI mutant. Characteristic retention time in HPLC of the different classes of carotenoids of lipophorin identified the presence of lutein as the major chromophore (62-77%), followed by beta-carotenes (22-38%). Although lutein and beta-carotene content of mutants' lipophorin differed significantly, the ratio of lutein to beta-carotene of 3:1 was not different among mutants. Similarly, lipid compositions of mutant silk glands were not significantly different, but carotenoid contents were. The significantly high concentration of lutein in the Y+I mutant silk gland represented more than 160-fold increase compared to +Y+I mutant (p<0.001). In this report, we conclude that lipid metabolism in the mutants is not defected and that the molecular basis for colorless hemolymph and cocoons is a defect in the cellular uptake of lutein associated with the Y-gene recessive mutants.
authors.affiliation: Division of Radiological Protection, National Institute of Infectious Diseases, Tokyo, Japan.
authors.forename: Kozo
authors.initials: K
authors.lastname: Tsuchida
authors.forename: Chihiro
authors.initials: C
authors.lastname: Katagiri
authors.forename: Yoshiro
authors.initials: Y
authors.lastname: Tanaka
authors.forename: Hiroko
authors.initials: H
authors.lastname: Tabunoki
authors.forename: Ryoichi
authors.initials: R
authors.lastname: Sato
authors.forename: Hideaki
authors.initials: H
authors.lastname: Maekawa
authors.forename: Naoko
authors.initials: N
authors.lastname: Takada
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Banno
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Fujii
authors.forename: Michael A
authors.initials: MA
authors.lastname: Wells
authors.forename: Zeina E
authors.initials: ZE
authors.lastname: Jouni
mesh_terms: D000818:Animals; D012831:Bombyx / Q000235:genetics / Q000378:metabolism*; D002338:Carotenoids / Q000378:metabolism*; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism; D002851:Chromatography, High Pressure Liquid; D002855:Chromatography, Thin Layer; D004591:Electrophoresis, Polyacrylamide Gel; D005088:Exocrine Glands / Q000378:metabolism; D006458:Hemolymph / Q000737:chemistry*; D005779:Immunodiffusion; D008074:Lipoproteins / Q000097:blood / Q000302:isolation & purification; D014975:Lutein / Q000378:metabolism; D009154:Mutation / Q000235:genetics*; D010858:Pigmentation / Q000235:genetics / Q000502:physiology*; D013997:Time Factors; D014304:Triolein / Q000378:metabolism / Q000493:pharmacokinetics; D014316:Tritium / Q000378:metabolism
chemical_list: D002352:Carrier Proteins; D008074:Lipoproteins; C032830:lipophorin; D014316:Tritium; D014304:Triolein; D002338:Carotenoids; D014975:Lutein