The Role of Hklp2 in the Stabilization and Maintenance of Spindle Bipolarity

Spindle bipolarity relies on a fine balance of forces exerted by various molecular motors [1–4]. In most animal cells, spindle bipolarity requires sustained outward forces to push the spindle poles apart, an activity that is provided by Eg5, a conserved homotetrameric plus-end-directed kinesin that...

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Bibliographic Details
Published in:Current biology 2009-11, Vol.19 (20), p.1712-1717
Main Authors: Vanneste, David, Takagi, Masatoshi, Imamoto, Naoko, Vernos, Isabelle
Format: Article
Language:English
Subjects:
Cell Line
Cell Polarity
CELLBIO
CELLCYCLE
Chromosomes, Human - metabolism
HeLa Cells
Humans
Kinesin - analysis
Kinesin - metabolism
Kinesin - physiology
Microtubules - chemistry
Microtubules - metabolism
Microtubules - ultrastructure
Models, Biological
RNA Interference
Spindle Apparatus - metabolism
Spindle Apparatus - physiology
Spindle Apparatus - ultrastructure
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Summary:Spindle bipolarity relies on a fine balance of forces exerted by various molecular motors [1–4]. In most animal cells, spindle bipolarity requires sustained outward forces to push the spindle poles apart, an activity that is provided by Eg5, a conserved homotetrameric plus-end-directed kinesin that crosslinks and slides antiparallel microtubules apart [5]. These pushing forces are balanced by inward minus-end-directed forces. Impairing both Eg5 and dynein restores the formation of functional bipolar spindles [4], although the mechanism at play is far from clear. The current model also fails to explain why in some systems Eg5 inhibition does not promote bipolar spindle collapse [6, 7] or why increasing Eg5 levels does not interfere with bipolar spindle assembly [8]. Moreover, the C. elegans Eg5 ortholog is not required for bipolar spindle formation [9]. We show here that the kinesin Hklp2 participates in the assembly and stabilization of the bipolar spindle. Hklp2 localizes to the mitotic microtubules in a TPX2-dependent manner and to the chromosomes through Ki67. Our data indicate that its mechanism of action is clearly distinct from and complementary to that of Eg5, providing an additional understanding of the mechanism driving the formation and maintenance of the bipolar spindle.
ISSN:0960-9822
1879-0445
DOI:10.1016/j.cub.2009.09.019