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Gene Behind Lincoln’s Diseas

the Utah biologists used mutant nematode worms lacking beta spectrin. The study focused on how the protein's absence affected axons, which carry nerve signals away from the nerve cell "body" and toward the synapse( the junction with another nerve cell).

The researchers used microscopes to photograph nerve-cell axons by inserting a jellyfish gene into the worms to make the worms' neurons glow fluorescent green.

The neurons were examined at three stages: as embryos, just after the worms hatched and at one day of age. The worms and their nerve cells still were growing during the first two stages.

It was found the nerves did not break in younger worms,so beta spectrin is not required for normal nerve growth and development, but is needed for preventing breakage of mature neurons, Hammarlund says.

In another experiment, the biologists paralyzed the worms by disabling two genes needed for muscles to contract. "In paralyzed worms, the axons do not break, even in the absence of spectrin, which says it is movement that causes the nerve cells to break, rather than continued growth of the animal," Jorgensen says.

That means beta spectrin normally prevents breakage by protecting neurons from the strain of movement, and not by helping add new membrane to a growing nerve cell.

"Everybody focuses on the synapse or the cell body as to where the action is," he says. "But if you break the wire or axon, the neuron doesn't work anymore. It's sort of the weakest link in the process."

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