Gardel et al. have discovered a perplexing anomaly regarding actin dynamics and cell traction on its extracellular matrix.
In a migrating cell, actin filaments polymerize at the leading edge, and flow back into the body of the cell (retrograde flow). It has been proposed that focal adhesions (FAs)—the cell's tether points to the extracellular matrix (ECM)—forming at the cell's leading edge provide handholds for the flowing actin that impede actin's retrograde movement, and in so doing create the traction needed to push the cell forward. The situation might be likened to a crowd of people being washed downriver and certain individuals gripping rocks (FAs) on the riverbed to work their way back against the flow.
Gardel et al. hypothesized that the speed of actin retrograde flow should be inversely correlated to traction force—the slower the river flows, the easier it is to grip the rocks and work one's way upstream—and indeed, this is exactly what they discovered. However, this was only true for the actin speeds seen at the front end of the cell (10–30 nm per second). At the frontal tip (where FAs are small), actin retrograde flow was rapid and traction was minimal. A little farther back in the leading edge (where FAs are bigger), traction increased and actin speeds slowed. Back toward the cell body, however, despite actin speeds dropping below 8–10 nm per second, the FAs exerted less traction.
Clare Waterman, who led the study, explains that the switch occurs roughly in the area where the lamellipodia (leading edge) ends, and the cell body begins. There must therefore be something different about the way the FAs and actin combine to generate tension in this region. RW