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Microtubule minus-end regulation at spindle poles by an ASPM-katanin complex

Kai Jiang1, Lenka Rezabkova2, Shasha Hua1

  • 1Cell Biology, Department of Biology, Faculty of Science, Utrecht University, Padualaan 8, 3584 CH Utrecht, The Netherlands.

Nature Cell Biology
|April 25, 2017
PubMed

Insights

The ASPM protein complex with katanin regulates microtubule dynamics at spindle poles. This interaction is crucial for cell division and preventing microcephaly, a brain development disorder.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • ASPM (abnormal spindle-associated protein male) is a microcephaly-associated protein family.
  • ASPM's role in spindle architecture is not fully understood.
  • Microcephaly is a neurological disorder characterized by a smaller than normal head size.

Purpose of the Study:

  • To elucidate the mechanism by which ASPM regulates spindle architecture.
  • To investigate the interaction between ASPM and katanin, another microcephaly-associated protein.
  • To understand how the ASPM-katanin complex influences microtubule dynamics.

Main Methods:

  • X-ray crystallography to determine the structure of the ASPM-katanin complex.
  • Reconstitution experiments to study protein interactions and functions.
  • Localization studies to observe protein distribution within the cell.

Main Results:

  • ASPM forms a complex with katanin, localizing mutually dependently to spindle poles.
  • The ASPM-katanin complex regulates microtubule dynamics and spindle flux.
  • ASPM inhibits microtubule minus-end growth, while katanin potentiates this effect and severs microtubules.

Conclusions:

  • The ASPM-katanin complex controls microtubule disassembly at spindle poles.
  • Misregulation of this complex can lead to microcephaly.
  • This study provides a mechanistic understanding of ASPM's function in cell division and development.

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