Ceiling Cat knows that we hardly need more evidence for evolution, but of course it just keeps pouring in, for Evolution is True. The latest piece—and it’s a nice one—is a report of “dead” genes (i.e., existing but nonfunctional genes) for taste receptors in some carnivores.
In WEIT, I mentioned how the presence of dead genes in some species, which have been inactivated by mutations and don’t make a protein product, can be explained only if those genes were active in an ancestor. Such genes include olfactory receptors in aquatic mammals (who don’t need them, since they can’t smell in air) and the final gene in the pathway for synthesizing vitamin C, which is dead in humans (we get enough vitamin C in our diet) but functional in our mammalian relatives. No creationist “theory,” save that of a Cosmic Trickster, can explain why a designer would put nonfunctional genes into the genomes of plants and animals.
The latest discovery is given in a paper published in PNAS (reference below) by Peihua Jiang and colleagues from the Monell Chemical Senses Center in Philadelphia and the Anthropological Institute and Museum at the University of Zurich. They sequenced genes for taste-receptor proteins in 12 mammal species and, combining this data from earlier studies, shows that several species of carnivores have inactivated taste genes, and presumably can’t experience the taste sensations which those genes ultimately produce. And the particular genes that are inactive are ones that aren’t much use given the species’ diets.
Scientists have found that mammals can perceive five taste qualities:
- umami, a “savory” sensation involving the detection of certain amino acids and ribonucleotides
Each of these sensations has its own taste receptors in the “taste buds,” and the sweet, bitter and umami sensations are detected through the conjunction of foodstuffs with special receptor proteins in the buds. (Salty and sour detection works differently, through the direct action of food ions on the nervous system.) The researchers worked only with sweet, bitter, and umami genes, since those have well-defined functions. The genes for these have complicated names, but we’ll refer to them as S-, B- and U-proteins respectively.
The researchers sequenced some or all of these three genes in 12 species of mammals: the aardwolf, the Canadian otter, the spectacled bear, the raccoon, the red wolf, the sea lion, the fur seal, the Pacific harbor seal, the small-clawed otter, the spotted hyena, the banded linsang, and the fossa. Here are the three you might not know:
We have known for a while that housecats and other felids lack functional sweet receptors, so when you feed your kitteh ice cream, it’s going for the dairy taste, not the sweetness! The authors predicted that mutations that inactivated sweet receptors might be seen in carnivores other than cats, especially sea lions and dolphins, which have “an atrophied taste system, exemplified by few taste buds present in their lingual epithelium.” Those two groups also swallow their food whole, which the authors postulate would “minimize opportunities and needs for taste input.” If you are evolved to go after anything that looks like a fish, then you don’t need to know how it tastes.
The general result is that taste receptor proteins are inactivated if the animal either doesn’t encounter that taste in their diet (and hence don’t need the receptors to ensure that they’re eating the right thing), or they eat by swallowing and not chewing chunks of meat, so there’s not a real need to taste the food:
- Sweet receptor genes that produce S-proteins are inactivated in the linsang, the fossa, the spotted hyena, the sea lion and fur seal, the Pacific harbor seal, and the asian small-clawed otter. All of these are either carnivores or piscivores (fish-eaters), and hence don’t encounter many sugars in their diets.
- There were all kinds of mutations inactivating the S-genes of these species: stop codons, insertions, nonsense codons, and deletions. And in each lineage the gene was inactivated independently since the disruptive mutations were different in different species. (The only exception was the S-genes in sea lions and fur seals, which are sister species who shared inactivating mutations that presumably occurred in their common pinniped ancestor. Since these genes don’t have much use in a meat- or fish-eater, mutations inactivating them presumably paid no selective penalty, or could have even been advantageous if they produced an “expensive” protein that was no longer needed. Earlier work also showed that the bottlenose dolphin also lacked functional S-genes.
Here’s a phylogeny of 18 species, with the red diamonds showing those species having inactive sweet-receptor proteins:
- The authors did taste tests on the otter and the spectacled bear to see if they could taste sugar: these involve giving the animals dishes of water containing sugar as well as control dishes containing either plain water or non-sweet chemicals. The otter had no preference, as one might expect since it has no sweet-receptor proteins, while the bear showed a strong preference for sugars (the bear is largely herbivorous and noms fruit, berries, cacti, and other plants with sugars).
- In sea lions and bottlenose dolphins, the umami receptors are also “dead,” and in the bottlenose dolphin the bitter gene also seems to be permanently broken. Those animals don’t chew their food, but rip off chunks and swallow them.
These results not only strengthen the already-airtight case for evolution and common ancestry, but show that whether taste genes are active or inactive depends on the animal’s diet, as one might expect. It also shows that gene loss in different lineages has occurred independently. I look forward to the Discovery Institute explaining this one (no worries—they’ll have a cockamamie explanation soon).
An interesting speculation, floated by my colleague Andrew Berry, is that the mutations inactivating taste receptors and olfactory receptors in humans (yes, we have some) have spread not because inactivated genes are selectively advantageous, but are actually “neutral” (i.e., have no effect on reproductive fitness). If that’s the case, then taste and smell genes could be polymorphic: some individuals might have active copies, other inactive ones. (“Neutral mutations” can hang around for long periods of time in a population.) This might explain why different people can taste and smell different things, and why some people, like wine- and perfume-testers, have extraordinarily keen abilities to detect scents and flavors. We know that there is polymorphism for genes affecting, for example, our ability to taste PTC, and for “how” we taste stuff like cilantro (I hate the stuff, as it tastes like soap to me; others love it).
As a sideline, the authors note that the sweet-receptor genes have also been inactivated in chickens, vampire bats, and “tongueless Western clawed frogs.” Taste tests show that neither chickens nor vampire bats can perceive sweetness (no sugar in blood!) but I found this sentence endearing:
“It is yet to be established how Western clawed frogs respond to sweeteners.”
Jiang, P., J. Josue, X. Li, D. Glaser, W. Li, J. G. Brand, R. F. Margolskee, D. R. Reed, and G. K. Beauchamp. 2012. Major taste loss in carnivorous mammals. Proc. Nat. Acad. Sci. USA online early edition, http://www.pnas.org/cgi/doi/10.1073/pnas.1118360109