Dynamics of Myosin II Filaments during Wound Repair in Dividing Cells

Md Istiaq Obaidi Tanvir1, Go Itoh2, Hiroyuki Adachi3,4

  • 1Graduate School of Sciences and Technology for Innovation, Yamaguchi University, Yamaguchi 753-8511, Japan.

Cells
|June 2, 2021
PubMed

Insights

Myosin II is not essential for cell membrane repair in dividing cells, as its dynamics at the wound site are calcium-dependent and not required for closure. This study reveals novel mechanisms of myosin II delocalization during cell repair.

Area of Science:

  • Cell biology
  • Biophysics
  • Molecular and cell dynamics

Background:

  • Cell membrane wound repair is vital for cell survival.
  • Myosin II's role in wound repair is established in larger cells but unclear in smaller, dividing cells.

Purpose of the Study:

  • To investigate the role of myosin II in cell membrane wound repair in dividing cells.
  • To elucidate the mechanisms governing myosin II dynamics at wound sites.

Main Methods:

  • Laserporation was used to induce wounds in the cell membrane of dividing cells.
  • Actin and myosin II dynamics were observed using live imaging.
  • Calcium influx and calmodulin inhibition were used to study regulatory pathways.
  • Myosin II-null cells were compared to wild-type cells.

Main Results:

  • Actin transiently accumulated, and myosin II transiently disappeared from the wound site.
  • Calcium influx triggered actin and myosin II dynamics, which were reduced by calmodulin inhibition.
  • Myosin II-null cells exhibited similar wound closure times to wild-type cells.
  • Myosin II delocalization occurred via a novel mechanism independent of phosphorylation-induced disassembly.

Conclusions:

  • Myosin II is not essential for cell membrane wound repair in dividing cells.
  • Calcium signaling and calmodulin play crucial roles in regulating myosin II dynamics during repair.
  • A novel mechanism governs myosin II delocalization from the cell cortex upon wounding.

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