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Coupling between microtubule sliding, plus‐end growth and spindle length revealed by kinesin‐8 depletion
Author(s) -
Wang Haifeng,
BrustMascher Ingrid,
Cheerambathur Dhanya,
Scholey Jonathan M.
Publication year - 2010
Publication title -
cytoskeleton
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.95
H-Index - 86
eISSN - 1949-3592
pISSN - 1949-3584
DOI - 10.1002/cm.20482
Subject(s) - anaphase , kinesin , biology , microtubule , microbiology and biotechnology , spindle apparatus , spindle pole body , mitosis , biophysics , genetics , cell division , cell cycle , cell
Mitotic spindle length control requires coordination between microtubule (MT) dynamics and motor‐generated forces. To investigate how MT plus‐end polymerization contributes to spindle length in Drosophila embryos, we studied the dynamics of the MT plus‐end depolymerase, kinesin‐8, and the effects of kinesin‐8 inhibition using mutants and antibody microinjection. As expected, kinesin‐8 was found to contribute to anaphase A. Furthermore, kinesin‐8 depletion caused: (i) excessive polymerization of interpolar (ip) MT plus ends, which “overgrow” to penetrate distal half spindles; (ii) an increase in the poleward ipMT sliding rate that is coupled to MT plus‐end polymerization; (iii) premature spindle elongation during metaphase/anaphase A; and (iv) an increase in the anaphase B spindle elongation rate which correlates linearly with the MT sliding rate. This is best explained by a revised “ipMT sliding/minus‐end depolymerization” model for spindle length control which incorporates a coupling between ipMT plus end dynamics and the outward ipMT sliding that drives poleward flux and spindle elongation. © 2010 Wiley‐Liss, Inc.