Figure 1

Fig. 1 Overexpression of STI1 protects both C. elegans and primary hippocampal mouse neurons from Aβ-toxicity. Sheet 1 a The average percent of dead cells ((# of dead cells)/(# of live + # of dead cells))x 100) in E17.5 primary hippocampal neuronal cultures from WT or TgA embryos. Cells were imaged in 4 well dishes from 8 random fields (N=6 individual embryos/genotype). Dishes were treated with either no Aβ, 0.1, 0.5 or 1 µM AβOs for 48 h. Sheet 2 b Likewise, WT or TgA primary hippocampal neurons were treated with 0, 0.25, 0.5 or 1 µM for 48 h, and LDH release was measured using colorimetric assay, read at 450 nm. N=3-4 individual embryos for WT hippocampal cultures for each condition and N=5 individual embryos per condition for TgA hippocampal cultures. Sheet 3 c Quantification of percentage of cell death in hippocampal neuronal cultures treated for 48 h with 1 µM scrambled Aβ control, antibody against STI1 (1:500), AβO alone (1 µM) or dishes treated with both AβO (1 µM) and anti-STI1 (1:500). At least four individual embryos were used for each condition and genotype. Sheet 4 d Percentage of body paralysis over 10 days in nematodes expressing Aβ(3-42) (strain CL2006 (dvIs2 [pcL12(unc-54/human Aβ peptide minigene)+pRF4]) in the bodywall muscle and treated with empty vector control RNAi, sti-1 RNAi, or hsp-90 RNAi. Sheet 5 e Percentage of paralysis in worms expressing Aβ3-42, Aβ3-42 worms overexpressing Hsp90 in body wall (strain AM988 (rmIs347(unc-54p::HSP-90::RFP)), Aβ3-42 worms overexpressing STI-1 in muscle cells (strain PVH40 (PPI1972 (unc-54p::STI-1::GFP);dvIs2))) and Aβ(3-42) worms overexpressing both STI-1 and HSP-90 in the bodywall muscle (strain PVH71 (rmIs347(unc-54p::HSP-90::RFP);(unc-54p::STI-1::GFP);dvIs2). For C. elegans experiments, 100 age synchronized animals were used for analyses.