GstS1M26 was generated through excision of GstS1EP1227 a genomic deletion that removes most of the GstS1 locus.
GstS1M26 mutants do not exhibit detectable neuron loss.
GstS1M26 is an enhancer of abnormal neuroanatomy phenotype of Hsap\SNCAUAS.cTa, Scer\GAL4ple.PF
GstS1M26 is an enhancer of abnormal neuroanatomy phenotype of park25
park25/Df(2R)ED1, GstS1M26 has short lived phenotype
GstS1M26 is an enhancer of dopaminergic neuron phenotype of Hsap\SNCAUAS.cTa, Scer\GAL4ple.PF
park25 mutants bearing the GstS1M26 mutation in trans with Df(2R)ED1 (in which GstS1 is deleted) are recovered at low frequency and display a dramatically shortened lifespan. Analysis of DA neuron integrity in 1-day old park25 mutants bearing this combination of GstS1 alleles reveals significantly enhanced DA neuron loss relative to park25 mutants. Loss of GstS1 function alone has no affect on DA neuron viability in 1-day old adults.
A GstS1M26 mutant background enhances the DA neuron loss found in flies expressing Hsap\SNCAScer\UAS.cTa under the control of Scer\GAL4ple.PF.
H.Benes