Gene mutation alters feeding behavior

DALLAS - Jan. 11, 2000 - A tiny transparent worm has enabled the first complete description of the biochemical steps leading from a genetic mutation to a change in behavior, UT Southwestern Medical Center at Dallas investigators reported in the December 24th issue of Science.

The understanding of the connection between genes and behavior at the molecular level is a major goal of neurobiology.

"A question we want to answer in looking at the human genome is what controls behavior," said Dr. Leon Avery, associate professor of molecular biology at UT Southwestern and senior author of the paper. "I believe a lot of the genetics of human behavior will be understandable in molecular terms through a change in a single ion channel or single receptor molecule."

The researchers studied a worm called a c. elegans that had a mutation that affected its feeding behavior. They showed that the mutation in the gene exp-2 caused an abnormality in a potassium channel so that it remained open rather than opening and closing normally. This alteration prevented opening of the pharynx, the muscle used to eat.

The opening of the potassium channel, called EXP-2, causes muscle relaxation. Normally the muscle relaxes a fifth of a second after contraction of the muscle. In the mutant worms, it relaxed in a 20th of a second after the contraction. This meant the muscle never contracted or opened all the way. The worms could not eat much because they could not take in adequate food.

"A good way to imagine this is that the pharyngeal muscle is like a pump, pumping food into the worm," Avery said. "It works very much like a human heart. If a heart pumps too fast, it can't really pump any blood before it starts to relax again."

Because the scientists were able to describe the biophysical, electrophysiological and behavioral effects of this mutation, they now know every step in the causal chain linking a mutation to altered feeding behav

Contact: Susan Steeves
UT Southwestern Medical Center

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