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A transposable genetic element associated with positive regulation of G6PD gene expression in Drosophila melanogaster

Published online by Cambridge University Press:  14 April 2009

Masanobu Itoh ,
Mari Iwabuchi ,
Naoki Yorimoto  and
Samuel H. Hori
Masanobu Itoh
Affiliation:
Department of Zoology, Faculty of Science, Hokkaido University, Sapporo 060, Japan
Mari Iwabuchi
Affiliation:
Department of Zoology, Faculty of Science, Hokkaido University, Sapporo 060, Japan
Naoki Yorimoto
Affiliation:
Department of Zoology, Faculty of Science, Hokkaido University, Sapporo 060, Japan
Samuel H. Hori*
Affiliation:
Department of Zoology, Faculty of Science, Hokkaido University, Sapporo 060, Japan
*
‡ Corresponding author.
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The DNA structures around the G6PD coding region in three high-G6PD activity mutants and their low-activity revertants of Drosophila melanogaster were analysed by Southern blot using a cloned G6PD gene as a probe. As a result, two kinds of insertion sequences were found; one was present just 5′ to exon I (Ins1), and the other within the intron (Ins2). The Ins1 sequence was 3·5 Kb in two mutants and 2·9 Kb in one mutant. In both cases, it consisted of a core sequence either 1·2 or 0·6 Kb long flanked by terminal repeats. On the other hand, low-activity revertants possessed either a defective Ins1 or no Ins1. The Ins2 sequence was found in all mutants and revertants, but not in Canton S. Although a recombinant phage carrying the DNA fragment spanning the entire Ins1 has not been obtained, sequencing data of the clone containing only the terminal repeats demonstrated that the repeats are defective P elements. Comparison of the genomic DNA structures of mutants and revertants suggested that the element responsible for the positive regulation of the G6PD gene in the mutants would probably be the core sequence, but not the flanking defective P elements. It was also conjectured that the 1·2 Kb core sequence might be composed of two identical elements, which might transpose independently.

Type
Research Article
Information
Genetics Research , Volume 52 , Issue 3 , December 1988 , pp. 169 - 177
Copyright
Copyright © Cambridge University Press 1988

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