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Heartless worms hold clues to cardiac arrhythmias, sudden death

ting factors -- are influencing HERG channel susceptibility to drug block.

That's where the worm came in. "This paper is really a proof of principle of the utility of using C. elegans to search for these HERG-interacting proteins," Petersen said.

Even though the worm doesn't have a heart, it does have a pharynx -- a muscular tube that "pumps" food inside. The pharynx, Petersen said, is similar in many ways to a heart. It has an intrinsic beating -- like a heartbeat -- that responds to neuronal input by speeding up or slowing down.

The investigators were able to take advantage of a worm line with a mutation in the worm version of HERG. The mutation, unc-103, causes profound neuromuscular defects, including a pharyngeal pumping defect that Petersen noticed as she learned to work with the worms.

"I remember the first time I saw it (the pumping defect)," she said. "It looked just like a cardiac arrhythmia." Whereas the normal worm pharynx has a rhythmic "beat" and rarely pauses, Petersen said, the unc-103 pharynx has long stretches of pauses, "as if the worms are having an arrhythmia."

The team developed a method to quantitate the pauses and demonstrated that "knocking out" the unc-103 protein using a technique called RNA interference restored normal pharyngeal pumping. The investigators reasoned that if they knocked out important HERG modulators, the effect would be the same: a restoration of rhythmic pharyngeal pumping.

To test this concept, they chose several candidate genes known to interact with HERG or other related potassium channels, knocked them out, and looked for improvements in the pumping defect. For two of the candidates, pumping improved -- the arrhythmia got better. One of these was a protein called KCR1, which Sabina Kupershmidt, Ph.D., assistant professor of Anesthesiology, and colleagues at Vanderbilt recently demonstrated prevents drug block of HERG in cardiac cells grown in the laboratory.
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19-Aug-2004


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