Lungs with taste, or lungs with a fortuitous receptor?

Researchers in Maryland have discovered an interesting quirk: lung smooth muscle expresses on its surfaces a protein that is the same as the bitter taste receptor. This could be useful, since they also discovered that activating that receptor with bitter substances causes the muscle to relax, opening up airways, and could represent a new way to treat asthma. That’s a fine discovery.

But man, it really tells us something about human psychology. I’m getting all this mail right now, and just about all of it asks the same question: Why do lungs have taste receptors? What is the purpose of sensing taste with the lungs? Even the investigators speculate this way:

Most plant-based poisons are bitter, so the researchers thought the purpose of the lung’s taste receptors was similar to those in the tongue — to warn against poisons. “I initially thought the bitter-taste receptors in the lungs would prompt a ‘fight or flight’ response to a noxious inhalant, causing chest tightness and coughing so you would leave the toxic environment, but that’s not what we found,” says Dr. Liggett.

Weird. I guess the teleological impulse really is etched deep into most people’s minds. I’m going to suggest that everyone just relax, let go, and embrace a simpler assumption.

There is no purpose.

That should be our default assumption. Gene regulatory networks are complicated, with expression of all kinds of genes coupled to other genes, so my first thought was that this was a simple biological accident, and totally unsurprising. I’ve looked at enough developmental gene expression papers to know that genes get switched on and off in all kinds of complicated patterns that have nothing to do with proximal function and everything to do with the network of connections between them; sometimes if gene A is active, the only ‘purpose’ is because A is coregulated by factor X which also switches on gene B, and B is the next step in a physiological or developmental program that is adaptive for the organism.

Another way to think of it: the handle on your teapot is wobbling loose, so you bring the home toolbox into the kitchen to tighten it up with your screwdriver. Your toolbox also contains wrenches and a hammer, but we don’t speculate that the reason you brought the hammer is that you need it right then to fix the teapot. The purpose of bringing the hammer is that it’s in the same handy toolbox as your screwdriver, which is not really a purpose at all.

Now the way evolution works is that this purposeless variation may fortuitously find a purpose — a gene in the T2R family of G-protein coupled receptors is uselessly misexpressed in the lungs, but a clever doctor finds a way to take advantage of it to treat asthma, or you may spot a vagrant mouse skittering across your kitchen counter, and suddenly the hammer becomes a useful implement of pest control — but the root of that innovation isn’t purpose, but purposelessness and serendipity.

There’s another reason to be unimpressed with the purpose of the expression of this gene in the lungs. Many of you may already be familiar with another quirk of the bitter receptor — its expression is variable in people. A common observation to make in genetics labs is the existence of non-tasters, tasters, and super-tasters to a substance called phenylthiocarbamide, or PTC. The mechanism of that is variability in this same kind of receptor gene now found to be expressed in lung tissue. Shouldn’t we be used to the random element of the expression of this gene by now?