The mitotic kinesin-14 Ncd drives directional microtubule-microtubule sliding

Research output: Contribution to journalResearch articleContributedpeer-review

Contributors

  • Gero Fink - , Max Planck Institute of Molecular Cell Biology and Genetics (Author)
  • Lukasz Hajdo - , Polish Academy of Sciences, University of Łódź (Author)
  • Krzysztof J. Skowronek - , Polish Academy of Sciences, International Institute of Molecular and Cell Biology in Warsaw (Author)
  • Cordula Reuther - , Max Planck Institute of Molecular Cell Biology and Genetics (Author)
  • Andrzej A. Kasprzak - , Polish Academy of Sciences (Author)
  • Stefan Diez - , Max Planck Institute of Molecular Cell Biology and Genetics (Author)

Abstract

During mitosis and meiosis, the bipolar spindle facilitates chromosome segregation through microtubule sliding as well as microtubule growth and shrinkage. Kinesin-14, one of the motors involved, causes spindle collapse in the absence of kinesin-5 (Refs 2, 3), participates in spindle assembly and modulates spindle length. However, the molecular mechanisms underlying these activities are not known. Here, we report that Drosophila melanogaster kinesin-14 (Ncd) alone causes sliding of anti-parallel microtubules but locks together (that is, statically crosslinks) those that are parallel. Using single molecule imaging we show that Ncd diffuses along microtubules in a tail-dependent manner and switches its orientation between sliding microtubules. Our results show that kinesin-14 causes sliding and expansion of an anti-parallel microtubule array by dynamic interactions through the motor domain on the one side and the tail domain on the other. This mechanism accounts for the roles of kinesin-14 in spindle organization.

Details

Original languageEnglish
Pages (from-to)717-723
Number of pages7
JournalNature cell biology
Volume11
Issue number6
Publication statusPublished - 2009
Peer-reviewedYes
Externally publishedYes

External IDs

PubMed 19430467
ORCID /0000-0002-0750-8515/work/142235570

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