Scientists Identify Gene Required for Nerve Regeneration |

A gene that is associated with regeneration of injured nerve cells has been identified by a team of researchers led by Prof Melissa Rolls of Penn State University.

The team has found that a mutation in a single gene can entirely shut down the process by which axons – the parts of the nerve cell that are responsible for sending signals to other cells – regrow themselves after being cut or damaged.

“We are hopeful that this discovery will open the door to new research related to spinal-cord and other neurological disorders in humans,” said Prof Rolls, who co-authored a paper published online in the journal Cell Reports.

“Axons, which form long bundles extending out from nerve cells, ideally survive throughout an animal’s lifetime. To be able to survive, nerve cells need to be resilient and, in the event of injury or simple wear and tear, some can repair damage by growing new axons,” Prof Rolls explained.

Previous studies suggested that microtubules – the intracellular ‘highways’ along which basic building blocks are transported – might need to be rebuilt as an important step in this type of repair.

“In many ways this idea makes sense: in order to grow a new part of a nerve, raw materials will be needed, and the microtubule highways will need to be organized to take the new materials to the site of growth,” Prof Rolls said.

The team therefore started to investigate the role of microtubule-remodeling proteins in axon regrowth after injury. In particular, they focused on a set of proteins that sever microtubules into small pieces. Out of this set, a protein named spastin emerged as a key player in axon regeneration.

Above: In fruit flies with two normal copies of the spastin gene, a team of scientists led by Prof Melissa Rolls of Penn State University found that severed axons were able to regenerate. However, in fruit flies with two or even only one abnormal spastin gene, the severed axons were not able to regenerate (Melissa Rolls / Penn State University)

Original paper here

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