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Positive regulation of the Drosophila melanogaster G6PD gene by a transposable element: its structure and function.

Positive regulation of the Drosophila melanogaster G6PD gene by a transposable element: its structure and function.
转座元件对果蝇 G6PD 基因的正调控:其结构和功能。
批准号:
63540499
负责人:
HORI Hiroshi
金额:
$1.22万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for General Scientific Research (C)
财政年份:
1988
资助国家:
日本
项目状态:
已结题
起止时间:
1988 至 1989

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中文摘要
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英文摘要
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.
期刊论文(11)
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Ito,H.: Sent to Biochemical Genetics.
Ito,H.:发送到生化遗传学。
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11
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