Illumination of the melanopsin signaling pathway
Melanopsin does not merely help with light sensing. It is a light sensor in its own right.
What this paper showed
By 2005 melanopsin was known to sit in the small group of retinal cells that report light to the body clock, and knocking it out was known to blunt the clock's response to light. But an open question remained, and it was the important one. Was melanopsin actually the light sensor, or was it a helper working alongside some other pigment that had not yet been found?
The way to settle this was to take melanopsin out of the eye entirely. The researchers put the melanopsin gene into cells that have no business responding to light and no other light sensing equipment of their own. Those cells then responded to light.
That is about as clean an answer as biology offers. Melanopsin alone was sufficient. Give it to a cell and the cell becomes light sensitive, which means the protein is a genuine photopigment rather than an accessory. The study also traced the chain of chemical events melanopsin sets off inside the cell once light hits it, and found it resembled the signalling used by invertebrate eyes more than that of our own rods and cones.
This is the paper that made melanopsin a target rather than a curiosity. Everything that followed, including molecules designed to block it and the research on how light quality and timing affect mood and sleep, rests on knowing that this one protein is where the process begins.
