The very first cold-sensing protein has been identified in the skin
For the first time, researchers have identified a protein in the skin that detects cold temperatures. The study was focused on the roundworm Caenorhabditis elegans. The team discovered that, without the receptor protein, the worms became completely insensitive to cold temperatures.
Study senior author Professor Shawn Xu is an expert at the University of Michigan Life Sciences Institute.
“Clearly, nerves in the skin can sense cold. But no one has been able to pinpoint exactly how they sense it,” said Professor Xu. “Now, I think we have an answer.”
Receptor proteins within the sensory nerves of the skin can detect when temperatures drop and signal information about this environmental change to the brain. The system works the same for humans as it does for the tiny, millimeter-long worm C. elegans.
“When you step outside and you sense it’s too cold, you’re going to take action to get back to a warmer environment as soon as you can,” explained Professor Xu. “When the worms sense cold, they also engage in avoidance behavior – moving away from cold temperatures, just like humans.”
Unlike complex organisms, however, C. elegans have a simple, extensively-studied genome and a short lifespan. This makes them the ideal model for investigating sensory responses.
According to Professor Xu, previous searches for a cold receptor have been unsuccessful because researchers were focusing on specific groups of genes that are related to sensation, which is a biased approach. The team in Professor Xu’s lab took an unbiased approach by looking across thousands of random genetic variations to determine which affected the worms’ responses to cold temperatures.
When temperatures dipped below 18 degrees Celsius, worms that were missing the glutamate receptor gene glr-3 no longer responded. This gene is responsible for making the GLR-3 receptor protein, which the researchers discovered is required for the worms to sense cold.
The study also revealed that the glr-3 gene is evolutionarily conserved across species, including humans. The researchers introduced the mammalian version of the gene to mutant worms lacking glr-3 and found that it rescued their cold sensitivity.
The team also introduced the worm, zebrafish, mouse, and human versions of the genes to cold-insensitive mammalian cells. Every version of the gene caused the cells to become sensitive to cold temperatures.
“For all these years, attention has been focused on this gene’s function in the brain. Now, we’ve found that it has a role in the peripheral sensory system, as well,” said Professor Xu. “It’s really exciting. This was one of the few remaining sensory receptors that had not yet been identified in nature.”
The study is published in the journal Cell.
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