| Project/Area Number |
63540499
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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 | Hokkaido University |
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Principal Investigator |
HORI Hiroshi Hokkaido University, Faculty of Science, Professor, 理学部, 教授 (40000814)
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| Co-Investigator(Kenkyū-buntansha) |
KIMURA Masahito Hokkaido University, Faculty of Science, Lecturer, 理学部, 講師 (30091440)
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| Project Period (FY) |
1988 – 1989
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| Project Status |
Completed (Fiscal Year 1989)
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| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1989: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1988: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | D. melanogaster / G6PD / Regulation of transcription / P elements / 遺伝子発現 / 動く遺伝子 |
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| Research Abstract |
Three high G6PD-activity mutants of D. melanogaster which have been found in a laboratory stock are characterized by two insertion sequences associated with the G6PD locus; one (Ins 1) is present just 5' to exon I and the other resides within an intron. The aim of the present project was to study the structure and function of the Ins 1 sequence. The following results were obtained: (1) The Ins 1 sequence consists of a core sequence flanked by a KP and KP' elements, and the sequence responsible for high G6PD activity may be the core sequence;(2) Cloning and sequencing data of the core sequence showed that this is another type of defective P elements(the internal sequence ranging from base 206 to base 2503 in the P element of p 25.1 is deleted); (3) The sequence spanning the junction of the 205th and the 2504th bases is unique to this particular type of P elements and may be capable of forming a palindrome in its central portion; (4) There is a protein in the nuclei of Canton S and mutant embryos that specifically binds to the core sequence; (5) The core sequence has a pair of DNase hypersensitive sites; (6) The transcription start site and the length of G6PD mRNA do not differ in wild-type and mutant stocks.
Based on these findings, it was concluded that insertion of a particular type of defective P elements in front of the G6PD coding domain provides the G6PD gene with a site to which a nuclear protein probably of regulatory function can bind, and hence, without disturbing the normal transcription machinery, results in the acceleration of transcription.
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