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

3株高G6 PD活性的D.已在实验室原种中发现的黑腹果蝇的特征在于与G6 PD基因座相关的两个插入序列;一个（Ins 1）仅存在于外显子I的5 ′端，另一个位于内含子内。本项目的目的是研究Ins 1序列的结构和功能。结果表明：（1）Ins 1序列由一个核心序列和一个KP和KP'元件组成，其中G6 PD活性高的序列可能是核心序列;（2）核心序列的克隆和测序数据表明，这是另一种类型的缺陷P元件（p25.1的P元件中从碱基206到碱基2503的内部序列被删除）;（三）跨越第205个和第2504个碱基的连接处的序列对于这种特定类型的P元件是独特的，并且可能能够形成一个互补序列。（4）在Canton S和突变体胚胎的细胞核中存在一种与核心序列特异性结合的蛋白质，（5）核心序列具有一对DNA酶超敏感位点;（6）G6 PD mRNA的转录起始位点和长度在野生型和突变型中没有差异。结论是，在G6 PD编码结构域之前插入特定类型的缺陷P元件为G6 PD基因提供了一个可能具有调节功能的核蛋白可以结合的位点，因此，在不干扰正常转录机制的情况下，导致转录的加速。

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.