This blog is a place where I will translate interesting findings in biomedical and basic science research from scientific jargon to plain old English. The bottom line: You don't need a PhD to understand science!

Friday, August 21, 2009

Early to bed, early to rise, makes a man healthy, wealthy, and A MUTANT?!

Your eyes meet. A foggy haze hangs in the air as you lean in for the kiss. Your lips are just about to touch, and the alarm goes off! We all know the feeling. Just ten more minutes!

For some, those ten minutes come after a comfortable seven to eight hours of sleep. For others, only six hours separates the night and the morning. While shorter sleep cycles lead to chronic sleep deprivation in a large percentage of the population, there are certainly individuals who find six hours of sleep sufficient. Why is it that a lucky few require only a fraction of the recommended seven to eight hours of sleep per night?

It looks as though the answer may reside once again in our DNA. In last week’s issue of Science Magazine, Ying He from the University of California at San Francisco reported that a small mutation in the DEC2 gene significantly decreases the length of a night’s sleep. He’s team identified the DEC2 mutation in two related individuals who indicated very early wake up times in a survey, reportedly sleeping nearly two hours less than other family members.

To study the significance of the DEC2 mutation on sleep cycles, He and colleagues generated transgenic mice that expressed the mutated human form of DEC2, called DEC2-P385R. He’s team found that mice expressing DEC2-P385R indeed had longer activity periods paired with shorter sleep phases. While many groups would be happily satisfied with this finding, He’s group took the experiment one step further. They next expressed the mutated mouse form of DEC2, called mDec2P38R, in fruit flies and recorded daily fruit fly activity. Remarkably, He found that mDec2P385R-expressing flies exhibited significantly less sleep-like behavior as measured by the duration of rest periods in light and dark conditions.

Not only did He’s study identify a sleep-specific behavioral function for the DEC2 gene, He's study also showed the remarkable conservation of DEC2 activity between vastly different species. While many genes are in fact shared between humans, mice, and flies, the amount of function that is retained for many genes is unclear. He and colleagues have now shown that DEC2 retains the ability to control sleep behavior in both the fly on your banana as well as in your neighbor next door.

Although this finding is fascinating, it is not yet a cause for jealousy over our peppy mutant friends. Many genes in our DNA carry out more than one function. Therefore, unknown consequences of the DEC2 mutation may yet remain hidden. Until we fully understand the spectrum of DEC2 actions, I wouldn’t be rushing to take a pill of DEC2-P385R.

The Bottom Line: The next time you’re late for work because you slept in, you can blame it on your DNA!

Reference: He et al. “The transcriptional Repressor DEC2 Regulates Sleep Length in Mammals. Science 14 August 2009: Vol. 325. no. 5942, pp. 866 – 870. DOI: 10.1126/science.1174443

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