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. 2005 May 23;102(22):8024–8029. doi: 10.1073/pnas.0501078102

Fig. 4.

Fig. 4.

GstS1 activity influences DA neuron viability in parkin mutants. (A)A GstS1 null allele (GstS1M26) in trans to a deletion (Df) of the GstS1 region [Df(2R)ED1] enhances DA neuron loss detected in the PPL1 cluster of 1-day-old parkin mutants. GstS1 null mutants (GstS1M26/Df) alone manifest no DA neuron loss in a WT parkin background. (B) Transgenic overexpression of GstS1 in DA neurons significantly suppresses DA neuron loss in 20-day-old parkin mutants (park25,TH-G4; UAS-GstS1). The degree of rescue conferred by GstS1 is comparable to that achieved by transgenic expression of parkin in DA neurons (park25,TH-G4; UAS-park). Statistical significance was calculated by using ANOVA and Bonferroni's post hoc test for planned comparisons. (*, P <0.05; **, P < 0.001; Δ, P = 0.3). Numbers shown in bars refer to the number of brains analyzed for neuron counts. park25 or parkrvA homozygotes were used in all analyses of neuronal viability.