Abstract
Epidermal closure of skin wounds on newt limb explants was inhibited to equal degrees by cytochalasins B,D and dihydiocytochalasin B (H2CB). The cytochalasin solvent, dimethylsulfoxide (DMSO), had no effect on migration at the low concentration present in the cytochalasin and control solutions. However, a 5% DMSO solution completely blocked mobility. Wounds on limb explants and limbs in situ responded similarly to cytochalasin treatment. Inhibition of migration by H2CB was reversible even when protein synthesis was reduced by 73%. Scanning electron microscopy of wound epithelium migrating on nucleopore filters revealed extensive lamellipodia on marginal cells and the first row of submarginal cells. Cytochalasin treatment produced plications in the upper surface and free edge of the normally smooth lamellipodia. This disturbance of the free edge revealed focal adhesions with the substratum. The fact that migration was inhibited by CD and H2CB (two cytochalasins with an affinity for contractile proteins but without some of the side effects of CB) leads us to conclude that epidermal cells utilize actin or actin-like proteins during wound closure. These results increase the likelihood that tissue cells of all types, whether in vitro or in vivo, share a common biochemical basis for cell movement.