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. 2017 May 24;10:154. doi: 10.3389/fnmol.2017.00154

FIGURE 8.

FIGURE 8

Deletion of glycine 116 does not perturb membrane-induced helix formation but does impair function in vivo. (A) Helix formation by the truncated CTD of wild-type (circles) and Δ116 (squares) worm CPX-1 upon addition of increasing concentrations of 85/15 POPC/POPS SUVs (blue), 85/15 POPC/POPS LUVs (green), 60/25/15 DOPC/DOPE/DOPS SUVs (black), or 60/25/15 DOPC/DOPE/DOPS LUVs (red) as monitored by CD spectroscopy. Comparable liposome conditions are grouped by color. Data for the wild-type protein are as reported previously (Snead et al., 2014), except that the data for wild-type CTD in the presence of DO SUVs was improperly normalized for protein concentration originally and has been renormalized here. (B) Aldicarb assays in wild-type, CPX-1 knockout (cpx-1), wild-type full-length rescue (FL), and Δ116 full-length rescue (ΔGly) demonstrating that deletion of Gly116 impairs the ability of CPX-1 to rescue aldicarb induced paralysis. Quantification is shown for paralysis at 60 min on aldicarb with number of trials annotated on each data bar. ∗∗Indicates a p < 0.01, based on a post hoc multi-comparison Tukey–Kramer test done after ANOVA.