High impact information on Zw

• While a null activity mutant allele of the structural gene for 6-phosphogluconate dehydrogenase in Drosophila melanogaster is lethal, a similar mutation for glucose-6-phosphate dehydrogenase is not [1].
• We propose that this excess divergence reflects episodes of natural selection on G6pd resulting in fixation of advantageous amino acid mutations in these two recently separated lineages [2].
• Two other enzyme loci exhibited a correlated variation with Adh-F--i.e., an increase of the S allele of glycerol-3-phosphate dehydrogenase (NAD+) (sn-glycerol-3-phosphate:NAD+ 2-oxidoreductase, EC 1.1.1.8) and of the F allele of glucose-6-phosphate dehydrogenase (D-glucose-6-phosphate:NADP+ 1-oxidoreductase, EC 1.1.1.49) [3].
• Alternative 6Pgd-G6pd genotypes are shown to differ in relative in vivo carbon flux through the pentose shunt [4].
• Restriction-map variation was studied in 126 copies of the G6pd region in X chromosome lines of Drosophila melanogaster from North America, Europe, and Africa. Special attention was focused on the distribution of variation relative to the geographically variable polymorphism for two electrophoretic variants [5].

Biological context of Zw

• There is strong linkage disequilibrium across the G6pd region [6].
• Nucleotide sequence of the Drosophila glucose-6-phosphate dehydrogenase gene and comparison with the homologous human gene [7].
• Restriction map polymorphism in a 13-kb region of the Zw locus in Drosophila melanogaster was investigated for 64 X chromosome lines with seven 6-cutter and ten 4-cutter restriction enzymes [8].
• The viability of different Zw genotypes is measured by examining whole chromosome viabilities relative to the FM6 balancer chromosome [9].
• Although a direct causative link could not be established, these results suggest an association between the amounts of quantitative and molecular genetic variation at the Zw locus region [8].

Anatomical context of Zw

• Using recombinant lines, we obtained data that suggested the existence of more than one gene on chromosome III involved in the regulation of G6PD in the fat body, and at least one of these genes affects the level of 6PGD as well [10].
• Confirmation that the Drosophila DNA fragment cloned in lambda DmG21 contains the G6PD gene sequence is based on the following observations. lambda DmG21 DNA shows hybridization only to the 18D region of the salivary gland X-chromosome, which is the known cytological locus for the G6PD gene [11].

Associations of Zw with chemical compounds

• The effect of DDT on the polymorphism at the G6pd and Pgd loci in Drosophila melanogaster [12].
• Targeted selection experiments and enzyme polymorphism: negative evidence for octanoate selection at the G6PD locus in Drosophila melanogaster [13].
• These differences in responses are localized in the fat body, with 300 mM sucrose in the diet resulting in a sixfold stimulation of G6PD activity and a fourfold one of 6PGD in the line showing the strongest response [10].
• Samples from the West Indies, Europe, and North America had a nucleotide diversity lower than that of African populations at vermilion and show nonequilibrium haplotype distributions at both vermilion and G6pd, consistent with a hypothesis of recent bottleneck and possibly also admixture in the history of these populations [14].
• The fragment DD5 is similar to glucose-6-phosphate dehydrogenase which provides NADPH to the cell [15].

Other interactions of Zw

• Females of the mex1 mutant strain show statistically significant elevated levels of the pentose phosphate shunt enzymes, glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase [16].

Analytical, diagnostic and therapeutic context of Zw

• In this report, we have analyzed the activation mechanism of the G6PD promoter by in vitro transcription and gel retardation assays [17].
• The chromosomal location of the genes for 6PGD and G6PD were determined by in situ hybridization to salivary gland polytene chromosomes [18].
• Southern blot analyses of revertants showing low G6PD activity suggested that the insertion sequence responsible for high G6PD activity may be the core sequence but not the flanking KP and KP' or the Ins2 [19].

References