Cells are always subjected to mechanical stresses, resulting in
wounds of the cell membrane, but cells are able to repair and reseal their wounded membrane. Previous reports have shown that actin and
myosin II accumulate around the
wound and that the constriction of this purse-string closes the membrane pore. Here, we developed a microsurgical
wound assay to assess
wound repair in Dictyostelium cells.
Fluorescent dye that had been incorporated into the cells leaked out for only 2-3 sec after wounding, and a GFP-derived, fluorescent Ca(2+) sensor showed that intracellular Ca(2+) transiently increased immediately after wounding. In the absence of external Ca(2+), the cell failed to repair itself. During the repair process, actin accumulated at the wounded sites but
myosin II did not. The
wounds were repaired even in
myosin II null cells to a comparable degree as the wild-type cells, suggesting that
myosin II does not contribute to
wound repair. Thus, the
actomyosin purse-string constriction model is not a common mechanism for
wound repair in eukaryotic cells, and this discrepancy may arise from the difference in cell size.