As you read these words a frenzy of activity is taking place as the light entering your eye triggers a dizzying sequence of actions, ultimately causing a signal to be sent to your brain. In fact, even a mere single photon can be detected in your vision system. It all starts with a photon interacting with a light-sensitive chromophore molecule. The interaction causes the chromophore to change configuration and this, in turn, influences the large, trans-membrane rhodopsin protein to which the chromophore is attached. This is just the beginning of the cellular signal transduction cascade.
The chromophore photoisomerization is the beginning of a remarkable cascade that causes action potentials to be triggered in the optic nerve. In response to the chromophore photoisomerization, the rhodopsin causes the activation of hundreds of transducin molecules. These, in turn, cause the activation of cGMP phosphodiesterase (by removing its inhibitory subunit), an enzyme that degrades the cyclic nucleotide, cGMP.
A single photon can result in the activation of hundreds of transducins, leading to the degradation of hundreds of thousands of cGMP molecules. cGMP molecules serve to open non selective ion channels in the membrane, so reduction in cGMP concentration serves to close these channels. This means that millions of sodium ions per second are shut out of the cell, causing a voltage change across the membrane. This hyperpolarization of the cell membrane causes a reduction in the release of neurotransmitter, the chemical that interacts with the nearby nerve cell, in the synaptic region of the cell. This reduction in neurotransmitter release ultimately causes an action potential to arise in the nerve cell.
All this because a single photon entered into the fray. In short order, this light signal is converted into a structural signal, more structural signals, a chemical concentration signal, back to a structural signal, and then back to a chemical concentration signal leading to a voltage signal which then leads back to a chemical concentration signal. There is, of course, a wealth of yet more detail which makes the information conversion process far more complicated.
Cellular signal transduction design is modular. Its many steps can be modified, or interchanged with alternative steps to provide solutions in other applications, such as the olfactory system. Within the vision system one can, for instance, modify the chromophore's color sensitivity—its action spectrum—so different colors cause their own specific signals.
An example of this is found in the so-called third eye (parietal eye) which is found in a variety of species. This eye is not an image forming eye but rather provides for light sensitivity. This system includes two antagonistic light signaling pathways in the same cell. Blue light causes the hyperpolarizing response as described above, but green light causes a depolarizing response.
How is this done? By the inhibition of the cGMP phosphodiesterase enzyme. Specifically, there are two opsins, one that is sensitive to blue light which activates the cGMP phosphodiesterase enzyme, and another that is sensitive to green light which inhibits the cGMP phosphodiesterase enzyme. It appears that initially these are two separate pathways and they come together at the point of influencing the cGMP phosphodiesterase enzyme.
The molecular components of this fascinating design are elucidated in a 2006 paper. In addition to reporting on their findings of this unique design, the final paragraphs propose an evolutionary explanation for the design. Here the paper turns from empirically based science to unfounded, non scientific speculation. Not surprisingly their evolutionary story begins with the heavy-lifting already accomplished and, in Lamarckian fashion, improvements are implemented as needed:
A G_o-mediated phototransduction pathway might already be present in the ciliary photoreceptors of early coelomates, the last common ancestor of lizard (vertebrate) and scallop (mollusk), because both have this pathway. Later, the ancestral vertebrate photoreceptor acquired a second G protein, either gustducin or transducin, for chromatic antagonism and perhaps other purposes. The parietal photoreceptor evolved subsequently and retained these ancestral features.
One can hardly blame evolutionists for their smuggling in of Lamarckian terminology. It sounds better than the Darwinian just-add-water account which holds that random biological variation produced a phototransduction pathway, and then produced myriad new proteins, which fortunately just happened to include a second G protein, which fortunately just happened to ... well you know the story.
