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. Author manuscript; available in PMC: 2019 Oct 10.
Published in final edited form as: Neuron. 2018 Oct 10;100(1):75–90.e5. doi: 10.1016/j.neuron.2018.09.014

Figure 1.

Figure 1

Biochemical characterization of αS multimers and cytotoxicity by individual E→K mutants. (a) Intact-cell crosslinking of αS using the cell-penetrant crosslinker DSG on M17D cells transiently expressing the indicated αS variants were lysed in PBS/1% Triton-X100; (b) αS60:14 ratios of all 5 genotypes by WB (Syn1) in n=7 ind. exps. (c-f): M17D cytotoxicity assays: (c) WB for cleaved PARP relative to the positive control (Bax); Ran is a negative control protein. n=3 ind. exps., each transfected as indicated, or mock (−); relative cleaved PARP is graphed in (d). (e) IncuCyte cell confluency assay and LDH-release cytotoxicity assay, n=11 ind. exps. (f) Correlation between decrease in T:M ratio and increase in LDH release. Means ± SD; n.s. non-significant; *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001, 1way-ANOVA, Dunnett’s multiple comparisons test.