Coupling between microtubule sliding, plus-end growth and spindle length revealed by kinesin-8 depletion

Haifeng Wang1, Ingrid Brust-Mascher, Dhanya Cheerambathur

  • 1Department of Molecular and Cell Biology, One Shields Avenue, University of California Davis, Davis, California 95616, USA.

Insights

Kinesin-8 depletion in Drosophila embryos causes excessive microtubule (MT) polymerization, leading to premature spindle elongation and altered MT sliding rates. This suggests a revised model for mitotic spindle length control.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Mitotic spindle length is crucial for accurate cell division.
  • Spindle length is regulated by microtubule (MT) dynamics and motor protein forces.
  • Kinesin-8 is a known MT depolymerase involved in spindle assembly.

Purpose of the Study:

  • To investigate the role of MT plus-end polymerization in mitotic spindle length control.
  • To examine the function of kinesin-8 in regulating MT dynamics and spindle length in Drosophila embryos.

Main Methods:

  • Studied kinesin-8 dynamics and inhibition using Drosophila embryo mutants.
  • Employed antibody microinjection to deplete kinesin-8.
  • Analyzed MT plus-end polymerization and interpolar (ip) MT sliding rates.

Main Results:

  • Kinesin-8 depletion led to excessive ipMT plus-end polymerization, causing overgrowth.
  • Inhibition of kinesin-8 increased poleward ipMT sliding rate, coupled with polymerization.
  • Spindle elongation occurred prematurely during metaphase/anaphase A and increased during anaphase B.

Conclusions:

  • Kinesin-8 plays a critical role in controlling MT polymerization at spindle poles.
  • A revised model incorporating ipMT plus-end dynamics and sliding explains spindle length control.
  • MT plus-end polymerization is a key factor in regulating spindle elongation rates.

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