Thursday, March 12th, 2015
Alex Mogilner (Suraneni et al) published a paper in Molecular Biology of the Cell, 'A mechanism of leading-edge protrusion in the absence of Arp2/3 complex‘ elucidating a novel myosin- and formin-dependent mechanism of cell motility.
Classical models of leading-edge protrusion rely on a Arp2/3-dependent treadmilling of dendritic actin network. However, in the absence of the Arp2/3 complex fibroblast cells maintain an ability to move. Joint work of Mogilner and Rong Li labs shows that cells extend formin-driven filopodia and build actin-myosin arcs in between filopodia, so that contraction of these arcs acting against membrane tension advances the cell leading edge.
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