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. 2012 May 1;23(9):1700–1714. doi: 10.1091/mbc.E11-11-0938

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© 2012 Reis et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 3: — Kinesin-1 reduction leads to impairment in retrograde APPYFP transport. (A) Distribution of retrograde segmental velocities. (B) Retrograde unweighted segmental velocity mode analysis for control shows three modes (cyan); see Table S1 for a definition of mode centers, spreads, and fractions of segment population. Superposition of modes is shown in red. (C) Analysis of retrograde duration-weighted segmental velocities shows a significant decrease in mean velocity for kinesin-1 reduction genotypes (mean μm/s ± SD): control, 1.02 ± 0.41; khc⁸/+, 0.65 ± 0.36; khc²⁰/+, 0.37 ± 0.19; klc^8ex94/+, 0.76 ± 0.39. (D) Decomposition of retrograde segmental velocity distribution into three modes for khc⁸/+. Although the centers of the three modes are similar to control conditions (compare with B), there is a significant shift of the vesicle population into mode 1 (see also Table S1). Red line, superposition of modes. A similar phenomenon is observed for khc²⁰/+ and klc^8ex94/+ (see Table S1). (E) Linear regression of retrograde velocity mode centers assembled for kinesin-1 reduction genotypes follows a ratio of ∼1:2:4.