Friday, November 9, 2012

Gene required for nerve regeneration identified

Photo Credit: Rolls lab, Penn State University

Scientists at Penn State and Duke University have identified a gene that is associated with the regeneration of injured nerve cells. The journal Cell Reports published an online early copy of their findings on Nov. 1, and will also include the paper in the monthly issue of the journal on Nov. 29. 


The team of researchers 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 –re-grow 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 Melissa Rolls, an assistant professor of biochemistry and molecular biology at Penn State, who led the research team, in a Penn State news release. 


“Axons, which form long bundles extending out from nerve cells, ideally survive throughout an animal's lifetime,” Rolls explained. “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.”


Earlier research suggests that microtubules, 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,” Rolls said. “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.”


Based on this research the team investigated the role of microtubule-remodeling proteins in axon re-growth after injury, focusing on a set of proteins that sever microtubules into small pieces. A protein named spastin emerged to play a critical role.


The team used fruit flies as their model organism to test the role of spastin. They found that in fruit flies with two normal copies of the spastin gene, 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.


"Now that we know that spastin plays an important role in axon regeneration and also that this gene is dominant, we have opened up a possible path toward the study of human diseases involving nerve-cell impairment," Rolls said. "In fact, our next step is to probe the link between hereditary spastic paraplegia (HSP) and axon regeneration."
 

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