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Don't hate those people who are perky and efficient after only a few hours of sleep. They can't help it. New research suggests that a genetic mutation may explain why some people sleep less.

In 2001, geneticist Ying-Hui Fu and colleagues identified a mutation in a gene called Per2 that appeared to cause Familial Advanced Sleep-Phase Syndrome (FASPS). People who have this condition sleep a normal 8 hours, but they go to bed earlier than most people, retiring at 6 or 7 in the evening and waking at 3 or 4 in the morning. "After that was published, a lot of these people with unusual sleep schedules came to us," says Fu, who is now at the University of California, San Francisco. " So we started to collect DNA samples." The team now has genetic information from more than 60 families.

Fu and her colleagues have spent the past several years mining this vast genetic storehouse for more mutations that might affect sleep patterns. In 2005, they uncovered another mutation associated with FASPS. And now they say they have found the first genetic mutation in humans that appears to affect sleep duration rather than sleep timing. The mutation lies in DEC2, a gene that codes for a protein that helps turn off expression of other genes, including some that control circadian rhythm, the internal clock that regulates a person's sleep-wake cycle. The mutation occurred in just two people, a mother and her daughter. The women sleep an average of only 6.25 hours, whereas the rest of the family members sleep a more typical 8 hours.

To confirm that this mutation shortens sleep, Fu and colleagues engineered mice to carry the mutant form of DEC2. The mutant mice slept about an hour less than normal mice, the team reports on 13 August in Science. The finding also held for fruit flies: Mutant flies slept about 2 hours less than normal flies.

DEC2 likely isn't the whole story when it comes to short sleep. "Genetic control of sleep is going to be complex and is going to include multiple types of genes," says Shaw, who was not affiliated with the study. But that doesn't diminish the importance of this paper, he notes. "It's really an amazing piece of work."

 "The findings", says Fu, "could lead to better treatments for sleep disorders". If the mutated form of DEC2 were available in a pill, Fu says she'd take it, noting that she needs about 8 hours of shuteye a night to feel rested. "All my life I've wanted to be able to sleep less."

1. Which of the following is true about the mutation in Per2 mentioned in the second paragraph?

A. It may explain why some people sleep less.

B. It may explain why some people sleep later.

C. It may explain why some people sleep longer.

D. It may explain why some people sleep earlier.

2. According to the passage, the mutated DEC2 ______.

A. was found from the people who contacted with FU voluntarily

B. was found at the same time when the mutated Per2 was found

C. was found to be associated with the FASPS

D. was found to be infectious in families

3. What is wrong with the mother and her daughter?

A. Their DEC2 doesn't code for the protein that turns off expression of the internal clock genes.

B. Their DEC2 codes for a protein that regularly turns off expression of the internal clock genes.

C. Their genes which directly control the internal clock are turned off with an irregular pattern.

D. Their genes which directly control the internal clock are turned off with a nontypical pattern.

4. Fu and colleagues changed flies' DEC2 ______.

A. to see whether it can carry the mutant form

B. to see whether the mutation causes short sleep

C. to see whether the mutation has more effect on flies

D. to see whether it controls the sleep cycle

5. What does Shaw think of DEC2?

A. It can't explain the short sleep.

B. It can explain the Short sleep very well.

C. It includes multiple types of genes.

D. It can't explain the short sleep alone.