Analysis of the effects of MOCS1 (Molybendum cofactor 1) upregulation on longevity in the fruit fly Drosophila melanogaster.

The purpose of this experiment was to test whether or not upregulating the MOCS1 gene in the fruit fly Drosophila melanogaster resulted in longer lifespan. This experiment used the UAS-GAL4 transgenic system to down-regulate ribosomal protein gene expression, which has been shown to lengthen lifespan in a wide range of organisms. The UAS-GAL system uses yeast GAL4 (not found in fruit flies) to drive expression of a transgene that either upregulates or downregulates a gene of interest. While the experiment showed increased lifespan in the experimental lines, there was also lifespan extension in a control that targeted GAL4 itself. All the GAL4 sensitive transgenes were integrated upstream of the MOCS1 gene, so we hypothesized that the lifespan extension observed in this previous experiment was due to inadvertent upregulation of the MOCS1 gene. MOCS1 is highly conserved among all taxa of life. When expressed, it produces an enzyme involved in synthesis of the Molybdenum Cofactor, which is part of an enzyme that removes toxic metabolites from cells. All the transgenic flies we used for this experiment were made isogenic to a background strain called w[1118]. One control group of flies had only the transgene ELAV, which expresses GAL4 in the nervous system. The other control had only a GAL4 sensitive transgene called EY00759, which is located in exactly the same place as the ribosomal transgenes used in the previous experiment, upstream of MOCS1 . The experimental group of flies had both transgenes, thus enabling MOCS1 to be upregulated. Every 2-3 days, we transferred the flies into new vials and recorded any deaths, which were plotted on survival curves using the lifespan analysis program DLife. In both males and females, the experimental flies lived significantly longer than the control groups.