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The mouse covers his eyes with his paw Credit: sibya via Pixabay
What makes a biological clock work? According to a new study from the University of Mississauga, the surprising answer lies in a gene generally badociated with stem cells and cancer cells.
In the first study of this type in the field of circadian biology, UTM researchers used RNA sequencing to observe expression of genes in the suprachiasmatic nucleus (NSC), a very small area of the brain hypothalamus that governs the mammalian biological clock. Their research highlights a gene that appears to regulate the biological clock and acts as a "master control" of the central circadian pacemaker.
Previously, researchers were studying Period2, a gene found in SCR, and were surprised to find that another gene called SOX2 was also present in the same region. "We found that Period2 was still expressed in the same cell population as those expressed in SOX2 – the biological clock was one of the major regions of the brain where these two genes were superimposed," says Hai-Ying. Mary Cheng, Associate Professor in the Department of Biology. Canada Research Chair in Molecular Genetics of Biological Clocks. "It's interesting because SOX2 is usually expressed in stem cells and cancer cells, but it's usually not found in large numbers in healthy brain brains or neurons. to have a function that nobody had thought of before. "
"Our research focuses on the basic understanding of how the body clock organizes," said the senior author and PhD. candidate Arthur Cheng (no relationship). He notes that events such as deep work, jet lag and time zone shifts can disrupt circadian rhythms in humans. "It can have a negative impact on health, it is thought that disturbed circadian rhythms are badociated with health problems such as fatigue, stroke."
Using mouse models lacking the SOX2 gene, the researchers observed rodent behavior under controlled environmental conditions. "A normal mouse with a working biological clock will start working as soon as the lights go off and turn on at night," says Arthur Cheng. "They stop and go to bed when the lights come on, but when we remove SOX2, the mice do not seem to know what they are doing."
"It's as if their clock was broken or outdated," adds Hai-Ying Mary Cheng. "He does not tell the time correctly." Mice lacking SOX2 also exhibited low functioning activity and irregular sleep patterns. "It was like they were jet lagged," Cheng said, noting that the microphone was also struggling to adapt to new schedules. "They lost their pace even with a small manipulation of light exposure," he says. "Jet lag adaptation is an integral part of our biological clocks, so we can survive intercontinental travel, but mice that do not have SOX2 are not able to adapt." . "
"When we removed SOX2, we observed significant changes in different SCN gene networks, which were very important to the functions of its neural network," said Hai-Ying Mary Cheng. "We believe that instead of regulating a single gene, SOX2 coordinates the expression of many genes and contributes to the function of the SCR as a regulator of circadianpacemaker."
The study was published in the March 2019 issue of Cell reports.
Explore further:
The research identifies a protein that regulates the biological clock
More information:
Arthur H. Cheng et al., SOX2-dependent transcription in clock neurons promotes robustness of the central circadian pacemaker, Cell reports (2019). DOI: 10.1016 / j.celrep.2019.02.068
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