Washington:
A team led by two Indian-origin scientists has identified a gene that regulates sleep and wake rhythms.
The discovery can provide potential therapeutic target to help night-shift workers or jet-lagged travellers adjust to time differences more quickly.
"It is possible that the severity of many dementias comes from sleep disturbances. If we can restore normal sleep, we can address half of the problem," said Satchidananda Panda, an associate professor at Salk Institute for Biological Studies in the US.
The discovery of the role of this gene, called Lhx1, can point to treatment strategies for sleep problems caused by a variety of disorders.
During the study, researchers disrupted the light-dark cycles in mice and compared changes in the expression of thousands of genes in the SCN with other mouse tissues.
The suprachiasmatic nucleus (SCN) is a small, densely packed region of about 20,000 neurons housed in the brain's hypothalamus.
They identified 213 gene expression changes that were unique to the SCN and narrowed in on 13 of these that coded for molecules that turn on and off other genes.
Of those, only one was suppressed in response to light: Lhx1.
"No one had ever imagined that Lhx1 - known for its role in neural development - might be so intricately involved in SCN function," added Shubhroz Gill, a postdoctoral researcher and co-first author of the paper.
Studying a mouse version of jet lag - an 8-hour shift in their day-night cycle -they found that those with little or no Lhx1 readjusted much faster to the shift than normal mice.
These mice also exhibited reduced activity of certain genes, including one that creates vasoactive intestinal peptide (Vip) - a molecule that has important roles in development and as a hormone in the intestine and blood.
"This approach helped us to close that knowledge gap and show that Vip is a very important protein. It can compensate for the loss of Lhx1," Panda said.
On the other hand, cutting back on Vip could be another way to treat jet lag, said the study that appeared in the journal eLife.
The discovery can provide potential therapeutic target to help night-shift workers or jet-lagged travellers adjust to time differences more quickly.
"It is possible that the severity of many dementias comes from sleep disturbances. If we can restore normal sleep, we can address half of the problem," said Satchidananda Panda, an associate professor at Salk Institute for Biological Studies in the US.
The discovery of the role of this gene, called Lhx1, can point to treatment strategies for sleep problems caused by a variety of disorders.
During the study, researchers disrupted the light-dark cycles in mice and compared changes in the expression of thousands of genes in the SCN with other mouse tissues.
The suprachiasmatic nucleus (SCN) is a small, densely packed region of about 20,000 neurons housed in the brain's hypothalamus.
They identified 213 gene expression changes that were unique to the SCN and narrowed in on 13 of these that coded for molecules that turn on and off other genes.
Of those, only one was suppressed in response to light: Lhx1.
"No one had ever imagined that Lhx1 - known for its role in neural development - might be so intricately involved in SCN function," added Shubhroz Gill, a postdoctoral researcher and co-first author of the paper.
Studying a mouse version of jet lag - an 8-hour shift in their day-night cycle -they found that those with little or no Lhx1 readjusted much faster to the shift than normal mice.
These mice also exhibited reduced activity of certain genes, including one that creates vasoactive intestinal peptide (Vip) - a molecule that has important roles in development and as a hormone in the intestine and blood.
"This approach helped us to close that knowledge gap and show that Vip is a very important protein. It can compensate for the loss of Lhx1," Panda said.
On the other hand, cutting back on Vip could be another way to treat jet lag, said the study that appeared in the journal eLife.
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