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Washington, Mar 11 (ANI): Johns Hopkins scientists have discovered that a light-sensing receptor that’s packed inside the eye’s photoreceptor cells is also critical for sensing temperature.

“For decades, this well-known molecule - one of the most-studied sensory receptors - was thought to function exclusively in the eye as a light receptor, but now we have found that fly larvae and possibly other organisms use it to distinguish between slight temperature differences,” says Craig Montell.

“And it makes you wonder about what was the more ancient role for rhodopsin - was it used originally for light or temperature detection?”

The team identified rhodopsin while investigating the process that results in the activation of a temperature-sensor protein known as a TRPA1.

Montell discovered earlier that TRPA1 enables fly larvae to detect tiny changes in the range of temperature that’s optimal for their survival. However, unlike TRP channels that function in avoiding hot and cold temperatures, TRPA1 was not directly turned on by changes in temperature in the comfortable temperature range, which extends from 18 to 24 degrees centigrade.

The team started looking for likely suspects in the large family of G-protein coupled receptors, because they are cell-surface molecules known to activate TRP channels.

“There were no precedents for a GPCR functioning in thermosensation, leaving us wonder where to start,” Montell says. “We considered rhodopsin, even though it was thought to be required exclusively for light reception, because some of the other proteins that we showed previously to function in thermosensation were required in photoreceptor cells.”

The researchers released about 75 larvae on a plate with two temperature zones; half of the plate was kept at their favorite temperature of 18 degrees C, and the other at an alternative temperature, ranging from 14 to 32 degrees C. After 10 minutes, the researchers counted the number of larvae that had crawled to the 18-degree side, and the number on the side with the alternative temperature.

They discovered that in contrast to the wild-type larvae, which preferred 18 degrees over any other temperature, the larvae lacking rhodopsin couldn’t discriminate temperatures in comfortable range, just like the larvae lacking TRPA1. However, the rhodopsin mutant larvae were able to choose 18 degrees over temperatures that were too hot or cold.

“The genetics and the behavior show that rhodopsin is required for thermosensation,” Montell says.

“Larvae that contain mutations disrupting rhodopsin are profoundly defective in their ability to sense temperatures, but only in the comfortable range. The simplest interpretation of these results is that rhodopsin is activated by temperature and this in turn, activates TRPA1. However, we cannot exclude that there is an additional accessory protein required for rhodopsin to act as a thermosensor.”

A report on the work appears March 11 in Science. (ANI)