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. 2010 Oct 5;68(9):1593–1610. doi: 10.1007/s00018-010-0535-z

Fig. 8a–e.

Fig. 8a–e

KLC1 mediates centrosome anchorage and functions in cell polarity. a and a′ KLC1 knock-down HaCaT cells (asterisks) stained for KLC1 and γ-tubulin exhibit increased centrosome–nucleus distances. Nuclei were stained with DAPI. b Statistical evaluation of control and KLC1-silenced cells illustrate a significantly (Student’s t test: P = 3.38 × 10−26) increased centrosome–nucleus distance in KLC1 mutants. Values are mean distances ± SEM. c and d Indirect immunofluorescence examination of control (c) and KLC1-silenced (d) cell monolayers 6 h post-wounding using antibodies against γ-tubulin and KLC1. Nuclei were visualized with DAPI. The dashed lines indicate the wound edge. Note that the centrosomes are not positioned towards the leading edge when KLC1 is absent. e Statistical evaluation of the representative experiments shown in c and d indicates defective cell polarization upon KLC1 knock-down. Centrosomes positioned within a 120° sector (dotted line) facing the wound were assessed as polarized. Results are the mean ± SD; Student’s t test: P = 3.03 × 10−3. Scale bars 10 μm