| Project/Area Number |
61540460
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
遺伝学
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| Research Institution | Okazaki National Research Institutes |
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Principal Investigator |
OKADA Kiyotaka National Institute for Basic Biology,Research Associate., 基礎生物学研究所・細胞生物学研究系細胞情報, 文部教官助手 (50101093)
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| Project Period (FY) |
1986 – 1987
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| Project Status |
Completed (Fiscal Year 1987)
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| Budget Amount *help |
¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1987: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1986: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | MHC class II genes / multigene family / polymorphism / repetitive sequence / chromosome walking / 主要組織適合抗原 / クロモソームウォーキング / 遺伝子クローニング / HLA遺伝子 / クラス【II】抗原 / 多重遺伝子 / クローニング |
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| Research Abstract |
Human MHC (Major Histocompatibility Complex) class II gene region is on the short arm of the 6th chromosome.More than 14 class II genes (6 <alpha>-chain genes and 8 <beta>chain genes) are clustered as <alpha>-<beta>gene pair in this region.Most of the genes are highly polymorphic in the human population.Immunological functions of the gene products are known to be differentiated.
This project aims to investigate the fine structure of the MHC class II multigene region and rationalize the possible mechanisms to generate this huge gene cluster accompanied by functional differentiation and high degree of polymorphism. Using the cosmid clones,I analyzed the organization of the gene pairs,and compared the homology between exons,introns and intergenic spaces,with several DNA probes including the Alu and kpn repetitive sequences. From these analyses, a model which involves gene duplications accompanied with some gene loss was proposed.
In order to investigate the functional difference between the class I antigens, cloned gene pairs'were transfered into mouse L cells, and assayed the stimulating. activities for IgG production and for T-cell activation (MLR).The DO gene products was shown to be different from the DR and DP gene products.Structural basis of the altered function of the DO gene pair was discussed.
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