Project/Area Number |
17580049
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Applied entomology
|
Research Institution | National Institute of Infectious Diseases |
Principal Investigator |
TSUCHIDA Kozo National Institute of Infectious Diseases, Division of Radiological Protection and Biology, Chief, 放射線管理室, 室長 (40231435)
|
Co-Investigator(Kenkyū-buntansha) |
FUJIMOTO Hirohumi National Institute of Infectious Diseases, Division of Radiological Protection and Biology, Senior Researcher, 放射線管理室, 主任研究官 (60373396)
|
Project Period (FY) |
2005 – 2006
|
Project Status |
Completed (Fiscal Year 2006)
|
Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2006: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2005: ¥2,200,000 (Direct Cost: ¥2,200,000)
|
Keywords | Bomby mori / Lutein / Carotenoid-binding protein / Mutant / Yellow blood gene / White blood gene / Transgenic / 細胞内透過機構 / リポホリン / カロチノイドの吸収 / カロチノイド結合タンパク質 / 遺伝子構造 / スプライシング / リボホリン / カロチノイドの細胞透過 / 突然変異体 |
Research Abstract |
The cDNA clone of CBP was obtained from the cDNA library of silk gland using anti-CBP antibody. The deduced amino acid sequence revealed that CBP is a novel member of the steroidogenic acute regulatory (StAR) protein family with its unique structural feature of a StAR-related lipid transfer (START) domain, known to aid in intracellular lipid transfer and recognition. These data suggest that CBP is a new member of the StAR protein family that binds carotenoids rather than cholesterol. CBP is expected to bind and shuttle carotenoids as an intracellular transporter and be one of the components that may make possible to tissue specific delivery of carotenoids. We obtained the evidence that the Y gene corresponds to the CBP gene. Restriction fragment length polymorphism (RFLP) mapping with a cDNA probe of the CBP gene revealed that the Y gene is on the same chromosome with the CBP gene. In the +^Y allele strain, an insertion of a retrotransposon and a partial ORF deletion occurred in the CBP gene locus. The absence of an exon, likely due to an incorrect mRNA splicing caused by the retrotransposon-associated genomic deletion, generates a nonfunctional CBP mRNA lacking the true start methionine. Consequently, CBP protein was only expressed in the Y allele strain. These data indicate that the CBP gene of the +^Y allele is a null allele, suggesting that the Y gene corresponds directly to the CBP gene. Transgenic expression of the CBP gene into a colorless hemolymph strain restored the yellow hemolymph and cocoons, thus verifying the function of CBP as the Y gene product.
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