The cells of your lungs express the same bitter taste receptor that is presence in the cells of your tongue (Deshpande et al., 2010). What's the reason for having these receptors in your lungs.
PZ Myers explains the concept of evolution by accident: Lungs with taste, or lungs with a fortuitous receptor?.
This is a very important concept and I'm delighted that PZ is promoting it. Adaptationists will not be happy. For more on this idea see: Evolution by Accident.
For more information about taste receptors see: Theme: A Sense of Smell/
Deshpande, D.A., Wang, W.C.H., McIlmoyle, E.L., Robinett, K.S., Schillinger, R.M., An, S,S,, Sham, J.S.K., Liggett, S.B. (2010) Bitter taste receptors on airway smooth muscle bronchodilate by localized calcium signaling and reverse obstruction. Nature Medicine. Published online October 24, 2010. [PubMed] [doi:10.1038/nm.2237]
10 comments :
Larry, Larry, Larry. Oh how you misunderstand. Of COURSE the taste buds in your lungs are an adaptive feature. They are there to give people drowning in soup something to focus other than their dying moments.
QED everything is adaptation.
Bitter taste receptors (TAS2Rs) on the tongue probably evolved to evoke signals for avoiding ingestion of plant toxins.
What a terrible way to start a scientific article!
Truti
Lar :
What's the reason for having these receptors in your lungs[?]
Dunno. But I bet it’s something you wouldn’t have thought of in a million years.
PZ Myers explains the concept of evolution by accident:…
Yeah, just like when the appendix was thought to have “evolved by accident,” then SHAZAAM! They found a function for it after all. But not to worry, just like with the appendix, you Darwinists will put an evolutionary spin on that, too. How wonderful it must be to be a slave to a “theory” that’s always right—even when it’s used to completely contradict itself!
Adaptationists will not be happy.
And when its subtly designed purpose is eventually discovered, neither will you Lar.
Of course, the adaptationists will rejoice in the fullness of evolutionary time, when our lung taste receptors acquire a function* by some fortuitous environmental change.
*acquire a function? Ugh, I sound like Haeckel talking about instinct: "a mental habit, acquired through adaptation, but then made heritable in the course of generations, appearing `native' in the end."
The reason? I guess it's because they happen to be next to a scrabble of DNA bases that somehow resemble what a transcription complex would call a promoter.
Geez, and then Nature rejects MY manuscripts...
Adaptationists are perfectly happy. There are hypotheses to test!
Of course, "pluralists" are always happy, because it's both the easiest thing in the world and all rigorously feel-good sciency to wave around your copy of Gould & Lewontin and shrug "accident" instead.
damn it. I meant to say:
WOTI?OK!
Sve says,
Adaptationists are perfectly happy. There are hypotheses to test!
That probably explains why so many evolutionary psychologists have grins on their faces.
Seriously, can you explain to me why adaptationists are never interested in testing non-adaptive hypothesies?
riiiight, because "adaptationist" = "evolutionary psychologist" *eyeroll*
But what the hell, I'll bite:
"can you explain to me why adaptationists are never interested in testing non-adaptive hypothesies?"
You're babbling. First, in any rigorous test for whether a phenotypic trait is adaptive, "no" is the null hypothesis, so in that sense it's tested every single time.
But that's not what's happening here. We're tallking about the expression of a membrane-protein receptor in a lung cell. What would a testable hypothesis of non-adaptation even look like?
Here, I'll try one prediction: If the protein is expressed accidentally and non-functionally, then I'd predict its presence or absence should have no functional consequences for the cells in qurstion.
Test: oops. This is not an orphan protein, sitting there with nothing to do, but rather it's hooked into a complete response cascade that causes the smooth muscle cell to contract when the receptor's chemical stimulus is present.
Prediction falsified, and it's not looking too good for the hypothesis that spawned it.
But I can think of testable funcional hypotheses all day long (my original point). How about you, Professor? How would you test your hypothesis that the expression of this protein in these cells is non-adaptive?
Sven says,
You're babbling. First, in any rigorous test for whether a phenotypic trait is adaptive, "no" is the null hypothesis, so in that sense it's tested every single time.
I agree with that. The default explanation has to be that the trait is not selected. But in most cases, the adaptationists conveniently forget to mention that they considered that possibility and rejected it for the following reasons ...
In most cases they act as though an adaptive explanation was the only possibility worth considering.
But that's not what's happening here. We're talking about the expression of a membrane-protein receptor in a lung cell. What would a testable hypothesis of non-adaptation even look like?
I'm not sure but I think it's worth considering the possibility that the trait nearly neutral BEFORE launching into an adaptive just-so story. That's the point that PZ was making. In other words, the first thing you have to do is provide evidence that the trait is adaptive.
One of the things I'd like to know first is whether the receptor is expressed in other mammalian lung cells. You could also do the knock-out in mice to see if it was important in all tissues. It might be possible to just block expression in the lungs and see what happens.
Until we have that kind of data I'd try to avoid jumping to conclusions. The first response of most people is to jump right over the default assumption and proceed to an adaptive explanation.
Here, I'll try one prediction: If the protein is expressed accidentally and non-functionally, then I'd predict its presence or absence should have no functional consequences for the cells in qurstion.
Test: oops. This is not an orphan protein, sitting there with nothing to do, but rather it's hooked into a complete response cascade that causes the smooth muscle cell to contract when the receptor's chemical stimulus is present.
Prediction falsified, and it's not looking too good for the hypothesis that spawned it.
I'm not sure that means anything. The proteins that mediate the response might already be present in lung muscle cells for other reasons. (I assume they're G proteins.)
But I can think of testable funcional hypotheses all day long (my original point). How about you, Professor? How would you test your hypothesis that the expression of this protein in these cells is non-adaptive?
I know you can think of adaptive hypotheses all day long. Adaptationists are very good at that. I've already given you some examples of experiments that are designed to test whether the receptor has a biological function of any kind. Once we have the answer to that question then you are free to make up hypotheses about WHY it has an important function.
jcc writes:
Yeah, just like when the appendix was thought to have “evolved by accident,” then SHAZAAM! They found a function for it after all.
Actually, what they found is that there are "good" microorganisms living there, which is true of pretty much every little cubic millimeter of your gut or the rest of your body. Then they speculate that this may give it the "function" of acting as a reservoir for these good microorganisms when they're mostly wiped out in the rest of the gut, after, e.g., a bout of cholera.
Now see, if I were designing an animal, I would design it not to get cholera in the first place. But hey, I know there's got to be a reason why the infinitely merciful and loving Designer designed us so millions upon millions of babies and toddlers throughout history died horribly from this disease, and perhaps you can tell me what that reason is.
And while you're at it - what's the design reason to give guys nipples?
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