14 DAY TRIAL // Do you go to sleep at the same time with the chickens?
Or are you a nigh bird?
Well, researchers have proven it to be hereditary.
In 2000, a family from Utah was found to be composed of early risers who slept from around five in the evening to two in the morning. The condition was named familial advanced sleep phase syndrome (FASPS) and gave scientists a chance to study the circadian rhythms to see how the body clock works, a tool for eventual therapies against seasonal affective disorders, jet lag and insomnia. A team at the University of California, San Francisco, has found in lab tests that the replacement of just one amino acid in a protein determines changes in the body clock's response to light and irregular sleep patterns. "A single amino acid change from serine to glycine, that's enough for all these people who have this mutation to have FASPS," says neurologist Ying-Hui Fu.
This change impedes a still unknown enzyme from adding a phosphate molecule onto the absent serine, which kicks off a domino effect resulting in lower overall transcription from DNA to mRNA (messenger RNA). This low mRNA level leads to lower amounts of protein when RNA is translated. "The message of this gene doesn't get transmitted appropriately," explains Fu," and therefore the protein level is low."
Other studies have hinted that the effect of Per2 gene (that encodes the protein) on the circadian rhythm was due to the protein stability, caused during or after translation. "The biggest surprise in this [study] was the change in messenger RNA as opposed to protein stability," notes University of Utah cancer and circadian rhythm specialist David Virshup. He also believes that post-translational effects are definitely not absent, based on the raw data.
The decrease in messenger RNA is only 30 % in the new study, while the protein decrease is of 80 to 90 %. "So, it's not just the transcription decrease. There must be some protein-stability effect, too", said Choogon Lee, a biomedical scientist at Florida State University
The team also added a mutated Per2 gene to mice, triggering a change in the animals' circadian period, sending them to sleep nearly two hours earlier than before. Deleting Per2 genes before inserting the mutation made the mice sleep and wake nearly four hours earlier than before. "The mutation has a dominant effect over the endogenous Per2, so without endogenous Per2, interference, the phenotype is worse," Fu says.
Inserting a copy of the gene that mimicked the effect of serine presence lengthened the circadian period. It "really tells you that this amino acid plays a really critical role. It's almost like a dial in your cell that can turn your [period] short or long." said Fu.
Developing therapies for scheduling the human body clock would eliminate problems from insomnia to seasonal affective disorder and cancer.