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Ca2+ signal blockers can inhibit M/A transition in mammalian cells by interfering with the spindle checkpoint

Naihan Xu1, Kathy Q Luo, Donald C Chang

  • 1Department of Biology, The Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong, PR China.

Biochemical and Biophysical Research Communications
|June 18, 2003
PubMed

Insights

Calcium signaling is crucial for cell division. Suppressing calcium levels disrupts the metaphase-anaphase transition by impairing the mitotic spindle checkpoint, highlighting calcium

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Sister-chromatid separation during the metaphase-anaphase transition is a critical event in mitosis.
  • Calcium (Ca2+) signaling has been implicated in regulating this process in somatic cells, but mechanisms remain unclear.

Purpose of the Study:

  • To investigate the effects of reduced cytosolic Ca2+ levels on mitosis.
  • To elucidate the role of Ca2+ in regulating the metaphase-anaphase transition and associated cellular events.

Main Methods:

  • Utilized GFP-gene fusion and living-cell imaging techniques in HeLa and PtK2 cells.
  • Applied the Ca2+ chelator BAPTA/AM to suppress cytosolic Ca2+ levels.
  • Observed the impact on mitotic spindle structure using YFP-labeled tubulin.

Main Results:

  • Suppression of Ca2+ by BAPTA/AM significantly blocked or delayed the metaphase-anaphase transition.
  • This blockage resulted from the failure to activate the anaphase-promoting complex (APC), preventing cyclin B and securin degradation.
  • Ca2+ suppression led to the gradual deformation of the mitotic spindle structure.
  • Other Ca2+ signal blockers, like heparin, produced similar inhibitory effects.

Conclusions:

  • Cytosolic Ca2+ is essential for the proper activation of the anaphase-promoting complex (APC) during mitosis.
  • Reduced Ca2+ levels interfere with the mitotic spindle checkpoint, leading to metaphase-anaphase transition failure.
  • Calcium signaling plays a vital role in maintaining mitotic spindle integrity and timely cell cycle progression.

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