Pilot screen for second site suppressors of wstd

Abstract

Triosephosphate isomerase (TPI) loss of function (wstd), in flies has been shown to have increases in methylglyoxal and advanced glycation end products (AGEs) which have also been found in increased levels in diseases such as Parkinson?s and Alzheimer?s disease. By showing that an increase in AGEs leads to neurodegeneration in drosophila, then the accumulation of AGEs might also be the cause of neurodegeneration in human diseases. This experiment is a pilot version of a screen looking for second site modifiers that interact with the TPI gene. A TPI rescue construct was performed from a cross with mutated male drosophila with a null allele for TPI with females deficient for TPI. The experiment selected for non-balancer phenotypes and restored viability in the F1 generation of the cross. The cross resulted in a low number of offspring, and no rescue phenotypes were observed. A fertility test showed that one possibility for the low number of offspring produced is that the mutant male drosophila had low fertility.