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A New Focus For The Mechanism Of Nerve Growth

dmill that is constantly being assembled at the leading edge and moved rearward, powered by a myosin II motor located at its back end. But, the networks making up this actin treadmill are constantly being recycled at the back end, and actin molecules are freed to complete a "virtual belt" cycle and be used again.

"Surprisingly, growth cones of nerve cells rapidly doubled in width when myosin II was blocked by blebbistatin," said Forscher. "FSM see that this was caused by inefficient recycling of actin filaments at the back end of the actin network treadmill."

Recycling of actin bundles at the ends of structures called filopodia was most strongly affected. This is important because filopodia are thought to play a key sensory role in growth cone guidance -- suggesting actin filament recycling and signaling may be intimately related.

The team is now investigating the implications of these findings for control of nerve growth, with particular interest in repair of spinal cord nerves after injury. Yale co-authors on the paper are Nelson A. Medeiros and Dylan T. Burnett. Support for the project was from the National Institutes of Health grant and the Nikon Partners-in-Research Program.

Citation: Nature Cell Biology: March 2006
(http://dx.doi.org/10.1038/Ncb1367)
Contact: Janet Rettig Emanuel
janet.emanuel@yale.edu
203-432-2157
Yale University

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