Fig. 2: Tm1 inhibits Khc motility via Khc’s regulatory tail.

a–c, Velocity of motile Khc complexes (a), frequency of processive Khc movements (b) and fraction of Khc microtubule-binding events that underwent processive motility (c) for Khc FL, Khc910, Khc940 and KhcΔAMB with or without Tm1 FL. Labeling efficiencies for Khc FL, Khc910, Khc940 and KhcΔAMB were 79.8%, 54%, 78% and 78.8%, respectively, so that total run numbers are underestimated. For all plots, the mean ± s.d. is shown and is derived from 162–2,185 individual complexes (a; N) or 16–59 microtubules (b,c; N) from 4–15 imaging chambers and 2–5 independent experiments (n) per condition (Supplementary Table 1). Mean values for each independent experiment (large dots) are superimposed on a violin plot showing the distribution of values from individual complexes (a) or on values for individual microtubules (small dots; b,c). Black or white circles indicate the presence or absence of the indicated components, respectively. Parallel experiments within the figure are shown with large dots of the same color. Cy3-osk 3′ UTR was included in all experiments. Statistical significance was determined by unpaired two-tailed Mann–Whitney test (a) or unpaired two-tailed t-tests with Welch’s correction (b,c) using N values (total number of individual complexes (a) or total number of microtubules (b,c)). NS, not significant (P > 0.05). Although Tm1 significantly increased the metrics of KhcΔAMB activity when comparing data that were aggregated between independent replicates, consistent effects were not seen between experiments. Data for Khc FL are reproduced from Fig. 1d–f.

Source data