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Published on: May 12, 2018
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.
Abstract:
Wound repair of cell membranes is essential for cell survival. Myosin II contributes to wound pore closure by interacting with actin filaments in larger cells; however, its role in smaller cells is unclear. In this study, we observed wound repair in dividing cells for the first time. The cell membrane in the cleavage furrow, where myosin II localized, was wounded by laserporation. Upon wounding, actin transiently accumulated, and myosin II transiently disappeared from the wound site. Ca2+ influx from the external medium triggered both actin and myosin II dynamics. Inhibition of calmodulin reduced both actin and myosin II dynamics. The wound closure time in myosin II-null cells was the same as that in wild-type cells, suggesting that myosin II is not essential for wound repair. We also found that disassembly of myosin II filaments by phosphorylation did not contribute to their disappearance, indicating a novel mechanism for myosin II delocalization from the cortex. Furthermore, we observed that several furrow-localizing proteins such as GAPA, PakA, myosin heavy chain kinase C, PTEN, and dynamin disappeared upon wounding. Herein, we discuss the possible mechanisms of myosin dynamics during wound repair.
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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