Wound Healing in Jellyfish Striated Muscle Involves Rapid Switching between Two Modes of Cell Motility and a Change in the Source of Regulatory Calcium

Small wounds (1.2 mm in diameter) made in the sheet of myoepithelial cells forming the 'swimming' muscle of the jellyfish, Polyorchis penicillatus, were closed within 10 h by epithelial cells migrating centripetally to the wound center. Some 24 to 48 h later these cells redifferentiated into fully contractile muscle cells. Labeling with bromodeoxyuridine failed to reveal any cell proliferation during this process. Phenotype switching (within 1 h) from contractile muscle cells to igratory cells did not require synthesis of new protein as shown by treatment with 40 [micro]M cycloheximide. Excitation-contraction coupling in undamaged muscle depended on entry of [Ca.sup.2+] through voltage-gated ion channels, as shown by a block of contractility by 40 [micro]M nitrendipine and also on calcium released from intracellular stores since caffeine (10 [micro]M) caused a 25% reduction in contractile force. In contrast, migratory cells did not require a source of extracellular calcium since migration was unimpeded by low (1 [micro]M) free [Ca.sup.2+] or nitrendipine. Instead, modulatory calcium was derived from intracellular stores since caffeine (10 mM) and thapsigargin (10 [micro]M) slowed migration. This lack of dependence on calcium influx in migratory cells was further confirmed by a dramatic down-regulation in voltage-gated inward current as shown by whole-cell patch recordings. Key Words: wound healing; striated muscles; cell motility; calcium; jellyfish.