A New Focus For The Mechanism Of Nerve Growth

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A New Focus For The Mechanism Of Nerve Growth

http://www.medicalnewstoday.com/medicalnews.php?newsid=39887

Researchers at Yale shed new light on the mechanism of nerve cell

growth by identifying novel functions for a molecular " motor "

protein, myosin II, according to an article in the March issue of

Nature Cell Biology.

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 Forscher

(http://www.biology.yale.edu/facultystaff/forscher.html), professor

of molecular, cellular and developmental biology at Yale

(http://www.biology.yale.edu/index.html) 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 to

prevent actin buildup that could actually impede neuronal advance. "

Forscher likened actin networks in the growth cone to a molecular

treadmill 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 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.