Additional file 1: of LMTK2 binds to kinesin light chains to mediate anterograde axonal transport of cdk5/p35 and LMTK2 levels are reduced in Alzheimer’s disease brains

Figure S1. siRNA knockdown of KLC1 and LMTK2 in rat cortical neurons. Knockdown of KLC1 does not affect expression of LMTK2, kinesin-1, KLC1, p35, cdk5 or tubulin. siRNA knockdown of LMTK2 in rat cortical neurons does not affect expression of kinesin-1, KLC1, p35, cdk5 or tubulin. siRNAs for LMTK2 and KLC1 have been described previously [27, 51]. Figure S2. Characterisation of KLC1-p35 PLAs in rat primary neurons. PLAs were performed with no primary antibodies, goat anti-KLC1 antibody alone, rabbit anti-p35 antibody alone or both KLC1 and p35 antibodies. Scale bar = 20 μm. Graph shows quantification of PLA signals in the different treated neurons. Neurons we also immunostained for tubulin to reveal neuronal architecture. Arrows show KLC1-p35 signals in axons. Data were analysed by Welch’s ANOVA and Games-Howell post hoc test; N = 25, ***p < 0.001. (DOCX 225 kb)