A taste receptor or tastant is a type of cellular receptor that facilitates the sensation of taste. When food or other substances enter the mouth, molecules interact with saliva and are bound to taste receptors in the oral cavity and other locations. Molecules which give a sensation of taste are considered "sapid".
Vertebrate taste receptors are divided into two families:
Visual, olfactive, "sapictive" (the perception of tastes), trigeminal (hot, cool), mechanical, all contribute to the perception of taste. Of these, transient receptor potential cation channel subfamily V member 1 (TRPV1) vanilloid receptors are responsible for the perception of heat from some molecules such as capsaicin, and a CMR1 receptor is responsible for the perception of cold from molecules such as menthol, eucalyptol, and icilin.
In 2010, researchers found bitter receptors in lung tissue, which cause airways to relax when a bitter substance is encountered. They believe this mechanism is evolutionarily adaptive because it helps clear lung infections, but could also be exploited to treat asthma and chronic obstructive pulmonary disease.
The sweet taste receptor (T1R2/T1R3) can be found in various extra-oral organs throughout the human body such as the brain, heart, kidney, bladder, nasal respiratory epithelium and more. In most of the organs, the receptor function is unclear. The sweet taste receptor found in the gut and in the pancreas was found to play an important role in the metabolic regulation of the gut carbohydrate-sensing process and in insulin secretion. This receptor is also found in the bladder, suggesting that consumption of artificial sweeteners which activates this receptor might cause excessive bladder contraction.
In addition, some agents can function as taste modifiers, as miraculin or curculin for sweet or sterubin to mask bitter.
Alternative candidate umami taste receptors include splice variants of metabotropic glutamate receptors, mGluR4 and mGluR1, and the NMDA receptor.
During the evolution of songbirds, the umami taste receptor has undergone structural modifications in the ligand binding site, enabling these birds to sense the sweet taste by this receptor.
Sensing of the sweet taste has changed throughout the evolution of different animals. Mammals sense the sweet taste by transferring the signal through the heterodimer T1R2/T1R3, the sweet taste receptor. In birds, however, the T1R2 monomer does not exist and they sense the sweet taste through the heterodimer T1R1/T1R3, the umami taste receptor, which has gone through modifications during their evolution. A recently conducted study showed that along the evolution stages of songbirds, there was a decrease in the ability to sense the umami taste, and an increase in the ability to sense the sweet taste, whereas the primordial songbird parent could only sense the umami taste. Researchers found a possible explanation for this phenomenon to be a structural change in the ligand binding site of the umami receptor between the sweet taste sensing and non-sensing songbirds. It is assumed that a mutation in the binding site occurred over time, which allowed them to sense the sweet taste through the umami taste receptor.
Signal transduction of bitter stimuli is accomplished via the α-subunit of gustducin. This G protein subunit activates a taste phosphodiesterase and decreases cyclic nucleotide levels. Further steps in the transduction pathway are still unknown. The βγ-subunit of gustducin also mediates taste by activating IP3 (inositol triphosphate) and DAG (diglyceride). These second messengers may open gated ion channels or may cause release of internal calcium. Though all TAS2Rs are located in gustducin-containing cells, knockout of gustducin does not completely abolish sensitivity to bitter compounds, suggesting a redundant mechanism for bitter tasting (unsurprising given that a bitter taste generally signals the presence of a toxin). One proposed mechanism for gustducin-independent bitter tasting is via ion channel interaction by specific bitter ligands, similar to the ion channel interaction which occurs in the tasting of sour and salty stimuli.
One of the best-researched TAS2R proteins is TAS2R38, which contributes to the tasting of both PROP and PTC. It is the first taste receptor whose polymorphisms are shown to be responsible for differences in taste perception. Current studies are focused on determining other such taste phenotype-determining polymorphisms. More recent studies show that genetic polymorphisms in other bitter taste receptor genes influence bitter taste perception of caffeine, quinine and denatonium benzoate.
It has been demonstrated that bitterness receptors (TAS2R) play an important role in an innate immune system of airway (nose and sinuses) ciliated epithelium tissues. This innate immune system adds an "active fortress" to the physical Immune system surface barrier. This fixed immune system is activated by the binding of ligands to specific receptors. These natural ligands are bacterial markers, for TAS2R38 example: acyl-homoserine lactones or produced by Pseudomonas aeruginosa. To defend against predators, some plants have produced mimic bacterial markers substances. These plant mimes are interpreted by the tongue, and the brain, as being bitterness. The fixed immune system receptors are identical to the bitter taste receptors, TAS2R. Bitterness substances are agonist of TAS2R fixed immune system. The innate immune system uses nitric oxide and defensins which are capable of destroying bacteria, and also viruses. These fixed innate immune systems (Active Fortresses) are known in other epithelial tissues than upper airway (nose, sinuses, trachea, bronchi), for example: breast (mammary epithelial cells), gut and also human skin (keratinocytes) Bitter molecules, their associated bitter taste receptors, and the sequences and homology models of bitter taste receptors, are available via BitterDB.
Free fatty acid receptor 4 (also termed GPR120) and to a much lesser extent free fatty acid receptor 1 (also termed GPR40) have been implicated to respond to oral fat, and their absence leads to reduced fat preference and reduced neuronal response to orally administered fatty acids.
TRPM5 has been shown to be involved in oral fat response and identified as a possible oral fat receptor, but recent evidence presents it as primarily a downstream actor.
type 1 (sweet) | TAS1R1 | GPR70 | 1p36.23 | TAS1R1/TAS1R3 heterodimers are the main umami taste receptor | Monosodium glutamate, Disodium guanylate, Inosine monophosphate, Guanosine monophosphate, (such as Beefy meaty peptide etc)Wu Y, Shi Y, Qiu Z, Zhang J, Liu T, Shi W, Wang X. Food-derived umami peptides: bioactive ingredients for enhancing flavor. Crit Rev Food Sci Nutr. 2024 Dec 10:1-17. | |
TAS1R2 | GPR71 | 1p36.23 | TAS1R2/TAS1R3 heterodimers are the main sweet taste receptor | (Glucose, Sucrose, Fructose etc), Aspartame, Carrelame, Cyclamate, Lugduname, Saccharin, Sucralose, Sucrononic acid, Sweet proteins (e.g. Brazzein, Curculin, Mabinlin, Monellin, Pentadin, Thaumatin etc) | ||
TAS1R3 | 1p36 | (Glucose, Sucrose, Fructose etc) | ||||
type 2 (bitter) | TAS2R1 | 5p15 | ||||
TAS2R2 | 7p21.3 | pseudogene | ||||
TAS2R3 | 7q31.3-q32 | |||||
TAS2R4 | 7q31.3-q32 | Denatonium, Quinine | ||||
TAS2R5 | 7q31.3-q32 | Quinine, Absinthin (selective) | ||||
TAS2R6 | 7 | not annotated in human genome assembly | ||||
TAS2R7 | 12p13 | Chloroquine | ||||
TAS2R8 | 12p13 | Denatonium | ||||
TAS2R9 | 12p13 | Denatonium, Quinine | ||||
TAS2R10 | 12p13 | |||||
TAS2R11 | absent in humans | |||||
TAS2R12 | TAS2R26 | 12p13.2 | pseudogene | |||
TAS2R13 | 12p13 | |||||
TAS2R14 | 12p13 | Flufenamic acid, TAS2R14 agonist 28.1 (selective) | ||||
TAS2R15 | 12p13.2 | pseudogene | ||||
TAS2R16 | 7q31.1-q31.3 | Denatonium, Amygdalin, Arbutin, Sinigrin, Salicin (selective) | ||||
TAS2R17 | absent in humans | |||||
TAS2R18 | 12p13.2 | pseudogene | ||||
TAS2R19 | TAS2R23, TAS2R48 | 12p13.2 | ||||
TAS2R20 | TAS2R49 | 12p13.2 | ||||
TAS2R21 | absent in humans | |||||
TAS2R22 | 12 | not annotated in human genome assembly | ||||
TAS2R24 | absent in humans | |||||
TAS2R25 | absent in humans | |||||
TAS2R27 | absent in humans | |||||
TAS2R28 | absent in humans | |||||
TAS2R29 | absent in humans | |||||
TAS2R30 | TAS2R47 | 12p13.2 | ||||
TAS2R31 | TAS2R44 | 12p13.2 | Acesulfame (in some individuals) | |||
TAS2R32 | absent in humans | |||||
TAS2R33 | 12 | not annotated in human genome assembly | ||||
TAS2R34 | absent in humans | |||||
TAS2R35 | absent in humans | |||||
TAS2R36 | 12 | not annotated in human genome assembly | ||||
TAS2R37 | 12 | not annotated in human genome assembly | ||||
TAS2R38 | 7q34 | Propylthiouracil, Phenylthiocarbamide, N-Acyl homoserine lactone | ||||
TAS2R39 | 7q34 | Denatonium | ||||
TAS2R40 | GPR60 | 7q34 | ||||
TAS2R41 | 7q34 | |||||
TAS2R42 | 12p13 | |||||
TAS2R43 | 12p13.2 | Denatonium | ||||
TAS2R45 | GPR59 | 12 | ||||
TAS2R46 | 12p13.2 | Denatonium, Oligoporins A-C, Oligoporin D (selective) | ||||
TAS2R50 | TAS2R51 | 12p13.2 | Amarogentin (selective) | |||
TAS2R52 | absent in humans | |||||
TAS2R53 | absent in humans | |||||
TAS2R54 | absent in humans | |||||
TAS2R55 | absent in humans | |||||
TAS2R56 | absent in humans | |||||
TAS2R57 | absent in humans | |||||
TAS2R58 | absent in humans | |||||
TAS2R59 | absent in humans | |||||
TAS2R60 | 7 | |||||
TAS2R62P | 7q34 | pseudogene | ||||
TAS2R63P | 12p13.2 | pseudogene | ||||
TAS2R64P | 12p13.2 | pseudogene |
The sweet taste receptor is one of the taste receptors where the function has been lost. In mammals, the predominant sweet taste receptor is the Type 1 taste receptor Tas1r2/Tas1r3. Some mammalian species such as cats and vampire bats have shown inability to taste sweet. In these species, the cause of loss of function of the sweet receptor is due to the pseudogene of Tas1r2. The pseudogenization of Tas1r2 is also observed in non-mammalian species such as chickens and tongueless Western clawed frog, and these species also show the inability to taste sweet. The pseudogenization of Tas1r2 is widespread and independent in the order Carnivora. Many studies have shown that the pseudogenization of taste receptors is caused by a deleterious mutation in the open reading frames (ORF). In a study, it was found that in nonfeline carnivorous species, these species showed ORF-disrupting mutations of Tas1r2, and they occurred independently among the species. They also showed high variance in their lineages. It is hypothesized that the pseudogenization of Tas1r2 occurred through convergent evolution where carnivorous species lost their ability to taste sweet because of dietary behavior.
Umami is also a taste receptor where the function has been lost in many species. The predominant umami taste receptors are Tas1r1/Tas1r3. In two lineages of aquatic mammals including dolphins and sea lions, Tas1r1 has been found to be pseudogenized. The pseudogenization of Tas1r1 has also been found in terrestrial, carnivorous species. While the panda belongs to the order Carnivora, it is herbivorous where 99% of its diet is bamboo, and it cannot taste umami. Genome sequence of the panda shows that its Tas1r1 gene is pseudogenized. In a study, it was found that in all species in the order Carnivora except the panda, the open reading frame was maintained. In panda, the nonsynonymous to synonymous substitutions ratio was found to be much higher than other species in order Carnivora. This data correlates with fossil records date of the panda to show where panda switched from carnivore to herbivore diet. Therefore, the loss of function of umami in panda is hypothesized to be caused by dietary change where the panda became less dependence on meat. However, these studies do not explain herbivores such as horses and cows that have retained the Tas1r1 receptor.
Overall, the loss of function of the a taste receptor is an evolutionary process that occurred due to a dietary change in species.
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