As nerve cells develop or attempt to recover after damage, they extend growth cones, highly flexible extensions that act as environmental sensors. Growth cones use the information they gather to direct advance of the nerve cells and it has long been known that such advance depends on the coordinated assembly of actin filament networks.
This study implicates the molecular motor, myosin II, as a key part of the process of recycling the actin networks and ultimately sensing and directing nerve growth.
Proteins in the Myosin family function as molecular motors; the most familiar myosins power contraction in heart and skeletal muscles. Myosin II motors are involved in functions such as directed cell movement, cell division and wound closure. While skeletal myosins have been studied in detail, non-muscle myosins are just beginning to be understood and this work identifies a new role for them.
The researchers, led by Paul Forscher, professor of molecular, cellular and developmental biology at Yale used a technique called fluorescent speckle microscopy, or FSM, that let them directly see actin filament assembly, disassembly and movement in living cells. They used FSM to monitor actin dynamics in nerve cells treated with a new drug called blebbistatin, that relaxes non-muscle myosin II and effectively blocks processes such as cell division.
"Past research has focused on how actin structures are assembled at the leading edges of motile cells," said Forscher. "Instead, this paper investigates turnover or recycling of the actin networks. As the complement to actin network assembly, recycling is necessary t