Pseudogenization of a Sweet-Receptor Gene Accounts for Cats' Indifference toward Sugar

Monell Chemical Senses Center, Philadelphia, Pennsylvania, USA.
PLoS Genetics (Impact Factor: 7.53). 08/2005; 1(1):27-35. DOI: 10.1371/journal.pgen.0010003
Source: PubMed


Although domestic cats (Felis silvestris catus) possess an otherwise functional sense of taste, they, unlike most mammals, do not prefer and may be unable to detect the sweetness of sugars. One possible explanation for this behavior is that cats lack the sensory system to taste sugars and therefore are indifferent to them. Drawing on work in mice, demonstrating that alleles of sweet-receptor genes predict low sugar intake, we examined the possibility that genes involved in the initial transduction of sweet perception might account for the indifference to sweet-tasting foods by cats. We characterized the sweet-receptor genes of domestic cats as well as those of other members of the Felidae family of obligate carnivores, tiger and cheetah. Because the mammalian sweet-taste receptor is formed by the dimerization of two proteins (T1R2 and T1R3; gene symbols Tas1r2 and Tas1r3), we identified and sequenced both genes in the cat by screening a feline genomic BAC library and by performing PCR with degenerate primers on cat genomic DNA. Gene expression was assessed by RT-PCR of taste tissue, in situ hybridization, and immunohistochemistry. The cat Tas1r3 gene shows high sequence similarity with functional Tas1r3 genes of other species. Message from Tas1r3 was detected by RT-PCR of taste tissue. In situ hybridization and immunohistochemical studies demonstrate that Tas1r3 is expressed, as expected, in taste buds. However, the cat Tas1r2 gene shows a 247-base pair microdeletion in exon 3 and stop codons in exons 4 and 6. There was no evidence of detectable mRNA from cat Tas1r2 by RT-PCR or in situ hybridization, and no evidence of protein expression by immunohistochemistry. Tas1r2 in tiger and cheetah and in six healthy adult domestic cats all show the similar deletion and stop codons. We conclude that cat Tas1r3 is an apparently functional and expressed receptor but that cat Tas1r2 is an unexpressed pseudogene. A functional sweet-taste receptor heteromer cannot form, and thus the cat lacks the receptor likely necessary for detection of sweet stimuli. This molecular change was very likely an important event in the evolution of the cat's carnivorous behavior.

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    • "aspects of digestive physiology. For example, cats lack a functional sweet taste receptor for detecting carbohydrate (Li et al. 2005) and, unlike other mammals, the induction of carbohydrases and monosaccharide transporters that occurs with carbohydrate feeding does not occur in cats (Buddington et al. 1991; Kienzle 1993). Consistent with the lack of sweet taste receptors, cats do not exhibit meaningful behavioural responses to sugars in the diet (Bradshaw et al. 1996). "
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    • "Conversely, animals lacking specific molecular machinery do not respond to certain stimuli. This is the case of a specialty feeder, the cat; Felidae have little need to handle carbohydrate, and it is interesting that they have lost functional expression of the carbohydrate-detecting sweet taste receptor (Li et al., 2005). Moreover, the induction of carbohydrases and monosaccharide transporters that occurs with carbohydrate feeding in omnivores does not occur in cats (Buddington et al., 1991; Kienzle, 1993). "

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    • "However, numerous pseudogenizations of taste receptor genes have been discovered in animals along with an increasing number of available genome sequences. For example, the sweet taste receptor gene (T1R2) is lost in the chicken, zebra finch, cat, vampire bats, and western clawed frog (Li et al. 2005; Shi and Zhang 2006; Zhao et al. 2010); the umami taste receptor gene T1R1 is lost in the giant panda, western clawed frog, and bats (Shi and Zhang 2006; Zhao, Yang, et al. 2010; Zhao et al. 2012). Strikingly, the draft dolphin genome (2.59× coverage) lacks intact genes responsible for sweet, umami, and bitter tastes (Jiang et al. 2012). "
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