Monday, July 25, 2005

Sweetness is wasted on cats

Cats, it turns out, can't taste sweet flavors. They have a genetic defect that renders them unable to perceive sweetness.

Cat owners have long recognized that, unlike most mammals, domestic cats are uniformly uninterested in sweet-tasting foods. According to an early study conducted at Monell in the 1970s, the same indifference to sweets is also evident in wild cats such as lions, tigers, leopards, and jaguars.

One interesting feature is that we have a chance to see how the theory of evolution can be brought to bear on this fact. Personally, on reading the lead-in to the article, I came up with three predictions:

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1: The genetic defect will be a break in a gene that builds part of the recepter for sweet flavors. That is, examination of the cat genome will show that, rather than being altogether absent, the gene is there, but it's broken.

2: Other cat species in which this indifference to sweets has been shown will turn out to have the same pattern of damage to the same gene.

3: If more than one gene is involved in the process,the other pieces will still be there, and still be functional in most of the species we investigate.

The hypothesis I'm working from here is that the affected cat species all descended from a common ancestor, and they inherited the same broken gene from that ancestor.

Intelligent Design/Intelligent Origin Theory, on the other hand, needs to explain why a genome with the shards of a broken gene left behind constitutes "intelligent design". Why build in a broken piece (and the rest of the pieces, if more than one piece is involved in the ability to taste sweet) instead of just leaving it out altogether? Why break this same piece in the same way in all these different species?

As it turns out:

The mammalian sweet receptor is composed of two protein subunits, known as T1R2 and T1R3. Each is coded for by a separate gene. In the new study, reported in the July 2005 inaugural issue of PLoS (Public Library of Science) Genetics, the researchers show a defect in the gene encoding the T1R2 protein in domestic cats.

OK, two parts. Interesting.

The Monell researchers also detected the same gene defect in tiger and cheetah, suggesting that it is common to species throughout the cat family. "This type of gene is known as a pseudogene and is somewhat like a molecular fossil," says Li. "It presumably once coded a functional protein, but no longer does so."

OK, the same defect, in different species within the family. Check.

Parallel studies showed that the defect is specific to the gene coding for the T1R2 protein, as the gene coding for the cat T1R3 protein is similar to those found in other mammals and appears to express a complete and functional protein.

The other piece, T1R3, is still present, despite being non-functional because of the absence of a working T1R2 gene. Check. Seems to be a silly design, if in fact it was designed. Evolutionary theory, on the other hand, has no problems with it.

Additional prediction: If another mammal in a different family is found which lacks the ability to taste sweet flavors, it will be due to a different defect – there's more than one way to break a system.

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