In these experiments, however, Van Gelder, and his research team demonstrated that the constriction of the pupil in the chick eye seems to be regulated by cryptochrome rather than melanopsin, Melanopsin is part of the family of proteins, called opsins, that mediate normal visual function. Most opsin proteins are located in the rods and cones of the eye’s retina. But the dissected chick eye had no rods or cones, and its response to light was different than a normal visual response.

In a series of experiments led by first author Daniel C. Tu, a graduate student in Van Gelder’s lab, the researchers looked at the chick eye under various kinds of light and treated it with drugs that disrupt normal, opsin-mediated visual pathways in insects and mammals. None of those experiments disrupted the pupil’s ability to constrict in response to light. But the researchers did get a response when they genetically manipulated the chick eye to reduce production of the cryptochrome protein.

When cryptochrome protein production was blocked by 50 percent, the researchers observed a corresponding 50 percent loss of sensitivity to light. Blocking production of melanopsin had no effect.

“This is still indirect evidence for the involvement of cryptochromes because in the chicken we can’t knock out or overexpress genes like we can in the mouse,” Van Gelder says. “But it does suggest cryptochrome proteins are involved.”

In both mice and chickens, Van Gelder says, it is as if the light meter of the eye is controlling the pupil without vision being involved. In the mouse, the meter is located in the retina and primarily uses melanopsin to do its work with cryptochrome proteins amplifying the signal. In the chick, it is as if the light meter is contained in the pupil itself.

It is not known if the nonvisual pathway seen in the embryonic chick eye is present in mammals. But even if human eyes do not use this particular light-mediated pathway, it still could have broader applications for human health.