Fig. 5.

Loss of membrane binding in the UNC-13 C-terminal domain does not impact nervous system function. (A) Average paralysis time course on 1 mM aldicarb for WT (black), ILL/AAA triple substitution mutant (AAA, orange), and artificial alpha helix substitution (hsHC2M, red) with the predicted AAA substitution location based on HC2M model (Inset). (B) Paralysis after 120 min for the same three strains as well as strains lacking either C2C (ΔC2C, cyan) or MCT (ΔMCT, green). (C) Tonic EPSCs were recorded from body wall muscle of adult worms in 1 mM external Ca²⁺. mEPSC traces from WT (black), AAA mutant (orange), and hsHC2M (red). Average of the frequency (D) and amplitude (E) of the mEPSCs from the same genotypes. (F) Representative stimulus-evoked EPSCs for WT (black), AAA (orange), and hsHC2M (red). Average EPSC peak amplitude (G) and cumulative charge transfer (H) for the same three genotypes. (I) First predicted alpha helix in MCT and a plot of the predicted alpha helicity for the WT helix (black) and artificial alpha helix substitution (red) using Agadir (68). (Inset) CD spectra for WT HC2M (black), AAA (orange), and hsHC2M (red). Strains: N2, JSD1193, JSD1200, JSD1288, and JSD1311.