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. Author manuscript; available in PMC: 2022 May 24.
Published in final edited form as: Curr Biol. 2021 Mar 24;31(10):2140–2154.e6. doi: 10.1016/j.cub.2021.02.061

Figure 3. AV transport is disrupted in human iPSC-derived LRRK2-G2019S knock-in neurons and rescued by LRRK2 kinase inhibition.

Figure 3.

(A) Kymographs of axonal EGFP-LC3 vesicles in WT and G2019S KI i3Neurons. See also Video S4. (B) Pause number, (C) Pause duration, (D) Fraction of time paused, (E) Number of reversals, (F) Δ run length of AVs in WT and G2019S KI i3Neurons (mean ± SEM; n = 133-189 AVs from 32-33 neurons from 3 independent experiments; ns = not significant, p=0.0299; ***p<0.0001; Mann-Whitney test with Bonferroni correction for multiple testing: p<0.0125 was considered statistically significant). (G) Kymographs of axonal EGFP-LC3 vesicles in G2019S KI i3Neurons treated overnight with DMSO or 100 nM MLi-2. (H) Pause number, (I) Pause duration, (J) Fraction of time paused, (K) Number of reversals, (L) Δ run length of AVs in G2019S KI i3Neurons treated with DMSO or MLi-2 (mean ± SEM; n = 225-279 AVs from 41-43 neurons from 3 independent cultures; ns = not significant, p>0.1368; **p=0.0021; ***p=0.0001; Mann-Whitney test). Dotted lines indicate the respective average in untreated WT i3Neurons.