Brown team enlists worms to link sleep duration to epigenetic tags

Brown University scientists linked epigenetic changes on the gene ZFYVE28 to short sleep in young adults. Now, they plan to determine if short sleep is a cause or effect of those changes.

What can worms and college students tell us about sleep? Plenty—with their help, Brown University scientists linked sleep duration in young adults to molecular changes in specific genes.

These changes, known as epigenetic tags, occur as a result of life experience, such as stress or exposure to certain substances. One type of epigenetic tag is DNA methylation, where methyl groups are added to the bases, or letters, in the DNA.

And while previous work has shown that lack of sleep might cause methylation at the whole genome level, the Brown team is the first to identify specific genes in which methylation patterns differ among people who get a normal amount of sleep and those who fall short.

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They collected blood samples from 16 students who participated in a sleep study. Half of them slept the recommended amount, while the other half were short sleepers, according to a statement. The team scanned hundreds of thousands of sites in the students’ DNA for methylation differences, finding 87 such aberrations on 52 genes.

The scientists turned to worms to model the effects of these epigenetic changes on sleep. They disrupted the genes they identified, landing on six that affected sleep in worms. When they looked at the DNA of a different group of students, they landed on one gene, ZFYVE28, that had “significantly different” methylation tagging in normal sleepers versus short sleepers.

The gene is associated with two molecular pathways known to play a role in sleep, but it is uncertain if the methylation changes are a cause or effect of short sleep, the team said in the statement. Their next step is to restrict the sleep of normal sleepers for a few weeks and then look at the ZFYVE28 gene for changes in methylation.

“Before this study, specific genes with epigenetic tags hadn’t been linked to how much sleep people get,” said Anne Hart, a professor of neuroscience and co-corresponding author of the study, published in the journal Sleep.

“In the long run, this work should help us understand why getting too little sleep causes so many problems for people and should lead to better treatments for those who have trouble sleeping,” Hart said.

While Hart’s team focused on epigenetics, other research has linked sleep quality to gene variants. A Washington State team knocked out a variant of the gene FABP7 in mice and found the mice slept more fitfully. Looking at a sleep study conducted in Japan, the scientists found that this translated into humans. And a group from Rockefeller University identified a gene variant that disrupts the body’s circadian clock. Patients with this variant produce more of a protein that keeps their “clock genes” off for longer than normal, so they tend to have delayed sleep phase disorder.

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