Institute for Bioengineering of Catalonia
Presented in the Embryo Physics Course, April 2, 2014
A fundamental feature of multicellular organisms is their ability to self-repair wounds through the movement of epithelial cells into the damaged area1,2. This collective cellular movement is commonly attributed to a combination of cell crawling and “purse-string” contraction of a supracellular actomyosin ring3-4. Here we show by direct experimental measurement combining traction and stress microscopy that these two mechanisms are insufficient to explain force patterns observed during wound closure. Contrary to common assumptions, we found that actin and myosin accumulate at the leading edge in a heterogeneous mechanical structure that transmits part of its tension to the underlying substrate through focal adhesions. The orientation of these adhesions and the traction forces they transmit are mainly parallel to the wound edge and thus perpendicular to the direction of cell motion. This structural and mechanical organization provides cells with an unanticipated mechanism to close the wound by cooperatively compressing the underlying substrate.