Correction appended
A team of researchers at Dartmouth Medical School has identified a gene that could be targeted to help jet-lagged travelers or workers on a late shift adjust their bodies' internal clocks to new schedules.
The team primarily studies the genetics and molecular biology of the circadian clock, a regulatory mechanism that drives many of the body's physiological processes including the sleep cycle, genetics department chair Jay Dunlap, one of the researchers involved with the study, said in an interview with The Dartmouth.
The researchers decided to investigate the gene, named Id2, after tests indicated that it could be involved in the circadian system.
The circadian clock dictates sleep patterns based on the natural light-dark cycle, Dunlap said, regardless of whether an individual is awake at night.
"Even though you're on shift work, it doesn't mean that the clock is resetting," he said. "The clock is being reset by the light-dark cycle, even when you're working. You're simply working when your brain is half-asleep."
The Id2 gene provides the genetic code for a protein that prevents other proteins from being produced, according to the study.
The team bred "knockout" mice that did not have the Id2 gene. These genetically altered mice, along with normal mice, were exposed to a disrupted light-dark cycle to examine the function of the protein produced by the Id2 gene.
"We discovered that the [mice without the gene] took only one or two days to recover from jet lag, while [mice with the gene] required the normal, longer four or five days to fully adjust," Giles Duffield, another of the study's authors, said in a press release. "It's like we removed the hand brake on their molecular machinery."
Duffield, who is now a biology professor at the University at Notre Dame, but was a research faculty member at DMS and the Norris Cotton Cancer Center at the time of the study, will likely conduct future research investigating how Id2 is involved in regulating the circadian system, Dunlap said, with the ultimate goal of determining the exact molecular mechanism involved.
"As soon as there's a real mechanism, then it's potentially druggable," Dunlap said.
Drug manufacturers may seek to develop a pill to allow people who need to adjust their internal clocks to do so more quickly, Dunlap said.
"All these disasters, Three Mile Island, Exxon-Valdez, Chernobyl -- all of these were the result of operator errors from people working late at night," he said. "We could design a pill so that when people went onto [a late shift], they might be able to reset their clock more quickly."
Dunlap said he was confident that the results of the study are applicable to humans.
"The circadian system in mice is quite similar to humans," Dunlap said. "I have every reason to believe that what we learned about the role of Id2 in mice will also be true in humans."
The study's results were published in the Feb. 24 issue of Current Biology.
Duffield could not be reached for comment by press time.
The original version of this article incorrectly stated that Giles Duffield, one of the study's authors, was a post-doctoral student at DMS at the time of the study. In fact, Duffield was a research faculty member at DMS and the Norris Cotton Cancer Center.
