| Project/Area Number |
04454205
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Immunology
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| Research Institution | (Institute of Immunological Science) Hokkaido University |
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Principal Investigator |
KAKINUMA Mitsuaki Hokkaido University Institute of Immunological Science, Professor, 免疫科学研究所, 教授 (00001735)
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| Co-Investigator(Kenkyū-buntansha) |
KODA Toshiaki University Institute of Immunological Science, Instructor, 免疫科学研究所, 助手 (20170186)
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥6,300,000 (Direct Cost: ¥6,300,000)
Fiscal Year 1993: ¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1992: ¥4,200,000 (Direct Cost: ¥4,200,000)
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| Keywords | Rat / MHC / RT1 / Class II genes / ラット / RT1.H / HLA.DP |
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| Research Abstract |
The present investigations deal with the identification and sturctural analysis of rat major histocompatibility complex, RT1, class II genes which remain to be identified. As results, we established the complete structures of three class II genes, RT1.Ha, RT1.Hb and RT1.DOa.
1.The RT1.Ha which is homologous to human HLA-DPA has intact DNA sequence. The expression is extremey low which was undetectable conventional Northern analysis. However, by polymerase chain reaction on rat splenic total RNA as a template, correctly spliced RT1.Ha mRNA was detected.
2.The TR1.Hb which is homologous to human HLA-DPB has a 7base pair deletion in the third exon generating a premature stop codon 13 codons thereafter, thus this gene is a pseudogene.
3.The RT1.DOa is the rat homologue of HLA-DNA and H-20a whose name was adopted at the nomenclatur committee according to our investigation. Messenger RNAs of both RT1.DOa and RT1.DOb were detectable in the spleen by Northern analysis.
4.RT1 probes are useful for detection of previously undetected MHC genes of rodents with human probes. One such example was the detection of putative H-2Pa sequence in the mouse which has been belived missing from the geneome of the mouse.
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