Plk1 negatively regulates NuMA cortical localization by phosphorylating at its C-terminus. Plk1 negatively regulates NuMA cortical localization by phosphorylating.

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Plk1 negatively regulates NuMA cortical localization by phosphorylating at its C-terminus. Plk1 negatively regulates NuMA cortical localization by phosphorylating at its C-terminus. (A–E) Images from time-lapse microscopy of HeLa cells stably expressing mCherry-H2B at metaphase, as indicated, transfected with various mutant forms of C-terminus (1,411–2,115) of NuMA (see text for details). The GFP signal is shown in green and the mCherry signal in pink. Please note significant enrichment in the GFP signal in cells expressing GFP-NuMAC-ter(SS1833/34AA) (B) in contrast to cells expressing either a wild-type NuMAC-ter construct or the other mutant forms. Quantification of cortical enrichment is shown below for 10 cells in each condition; (P < 0.005 for metaphase cells expressing GFP-NuMAC-ter(SS1833/34AA) in comparison with either GFP-NuMAC-ter or other mutant constructs as analyzed by two-tailed t test; error bars: SD). (F, G) Images from time-lapse microscopy of HeLa cells stably expressing mCherry-H2B and partly depleted of endogenous NuMA at metaphase or at various stages of anaphase, as indicated, transfected either with GFP-NuMA (F) or GFP-NuMA(SS1833/34AA) (G). The GFP signal is shown in green and the mCherry signal in pink. Please note significant enrichment in the GFP signal in a cell expressing GFP-NuMA(SS1833/34AA) in contrast to the wild-type GFP-NuMA. Quantification of the cortical enrichment shown on the right representing the cortical signal as cells are progressing from metaphase to anaphase transition. For cells undergoing metaphase to anaphase transition from −2 min to 6 min, the P < 0.05 for cortical GFP signal between GFP-NuMA and GFP-NuMA(SS1833/34AA) and P ≥ 0.1 for 8 to 12 min intervals between GFP-NuMA and GFP-NuMA(SS1833/34AA), as analyzed by two-tailed t test; error bars: SD). (H–K) Schematic representation of the mitotic spindle on an L-shaped micro-pattern as shown in Fig 3A. Spindle orientation was determined as an angle as depicted, with 0° being defined as the position of spindle along the hypotenuse as shown. (H–K) represents the frequency of angular distribution of spindle positioning every 15°. Note the change in the axis of the spindle orientation in cells weakly expressing GFP-NuMA(SS1833/34AA) (K) in contrast to the untransfected control cells (I) or cells weakly expressing GFP-NuMA (J) [N = 20 for untransfected, N = 15 for cells expressing GFP-NuMA, and N = 23 for cells expressing GFP-NuMA(SS1833/34AA)]. P < 0.005 between GFP-NuMA(SS1833/34AA)–expressing cells and untransfected control cells, or between GFP-NuMA and GFP-NuMA(SS1833/34AA)–expressing cells as calculated using two-tailed t test. (L) Model illustrating the impact of Plk1 on the cortical localization of NuMA and therefore dynein during metaphase. In control metaphase cells (on the left), spindle-pole pool of Plk1 (shown in yellow on the spindle-pole) creates a gradient (in red) and influences cortical dynein complex localization through phosphorylating NuMA (shown in orange). This process orchestrates the balanced levels of cortical levels of NuMA/dynein, which is essential for proper spindle orientation. Plk1 inactivation in metaphase (shown on the right), causes loss of negative regulation on NuMA and thus NuMA/dynein levels augment which causes to spindle orientation defects. Shrividya Sana et al. LSA 2018;1:e201800223 © 2018 Sana et al.