One Versus Many
In my last article, I presented a A Single-Protein Model of Music Perception. The essential details of the single-protein model are:
- The musicality condition is determined by the relative concentrations of two different molecular or ionic species in the extra-cellular medium (in the brain), where the two concentrations are function of local neural activity, but not exactly the same function in each case.
- Some transmembrane neuronal protein has its operation affected by the relative concentration (i.e. more of one species and less of the other), in a manner which increases the excitability of the neuron.
- The thus-excited neuron contributes to the emotional response to music, which ultimately modulates the memory for certain types of information.
I suggested that the protein in question would be a human-specific splicing variant of some known neuronal protein. Which raises the question: which protein is it? Which other protein is it a human-specific isoform of? And if we have to trawl through all the possibilities, how many are there? I.e., how many neuronal transmembrane proteins are there?
I'm not too sure of the exact answer, but I'm guessing in the hundreds. For example, search on Google for human neuronal transmembrane protein site:en.wikipedia.org, which returns 769 results, a significant portion of which are individual protein genes.
If we can't tell which one it is ...
Which leads to an interesting possibility. If we don't know which of these hundreds of proteins make music perception happen, maybe all of them do.
In other words, instead of there being one human-specific variant protein, which is majorly responsible for music perception, maybe there have been hundreds of minor variations in different proteins, each of which contributes a small component of music perception. In each case, the variation interferes only slightly with the protein's normal function, and the sum of contributions is strong enough to give rise to music perception as we experience it.
This would perhaps be somewhat unusual in biology, where identifiable functions generally have an identifiable implementation, and any particular task is performed by a small set of specific components.
Plausibility of a Super-Multi-Protein Model
However, the alleged function of music perception does have certain properties which make a super-multi-protein implementation of a musical information circuit plausible:
- The source of information is one-dimensional and spread over a certain region of the brain (i.e. a subset of regions which play some role in speech perception).
- The target of the information is also one dimensional, i.e. to what extent certain types of information should be remembered.
- The information is only required to be signalled correctly on average over the long term, i.e. there is no requirement for short-term accuracy of transmission.
Given this requirement, for each protein exposed to information about the musicality condition, we can ask, is there some minor variation in that protein, which can cause its operation to be slightly affected by the musicality condition, in such a manner that the memory for the required type of information is on averaged slightly increased by the changed operation of the protein?
For each protein, if the answer is yes, then there will be a selective pressure acting on the gene determining that protein, and it will evolve accordingly.
Furthermore, for each protein, the selective pressure will be limited once the selected-for variation starts to interfere significantly with the protein's normal function.
Predictions of the Multi-Protein Theory
One consequence of this theory is that it will be almost impossible to identify any one specific genetic cause of human musicality, and in this sense it is almost unscientific. (The theory is not totally unpredictive, because it still predicts the eventual observation of constant activity patterns when perceiving music, when the technologies available to observe human brain activity permit a sufficient degree of spatial resolution.)
On the other hand, such a theory does account for the observed robustness of music perception, in the sense that there is little evidence of any genetic condition which specifically affects music perception, and music perception is also relatively unaffected by mind-altering drugs. This is what we would expect if the implementation of music perception is spread over a large number of neuronal proteins, i.e. a mutation in any one individual protein or interference in the operation of any one individual protein will have little effect on music perception.
Furthermore, as I have mentioned previously, when amusia does occur, it appears to be caused by a deficiency in the prerequisite low-level perceptions required to perceive music, i.e. discrimination of pitch and (sometimes) discrimination of time. To give a simple analogy, it's like a car where the engine was so tough and unbreakable that the only reason the car ever failed to work was because the wheels had come off.
It is even possible that amusia caused by failure in pitch discrimination is a secondary evolved adaptation to reduce music perception, perhaps as part of an evolutionarily stable strategy where it benefits some maximum portion of the population. In other words, music perception has evolved via minor alterations in many different genes, but if selective pressure occurs to reduce music perception, then the quickest way to effectively sabotage music perception will be to alter a smaller set of genes which determine the quality of raw information coming in to those parts of the brain where musicality is computed.