An estimated 80% of what people refer to as “taste” is actually the sense of smell.  The taste buds of the tongue do not taste chocolate (other than the sweetness of it) or spaghetti sauce (other than the salty and sour nature of it).  We do not identify cheese, or wine, or most other foods by their tastes, but by their smells.  When one holds his/her nose, he/she loses much of their ability to “taste”.  The sense of taste is far more pragmatic than the nose (which can distinguish between different kinds of cheese, wine, etc.).  Once something has been put into the mouth, there is a very short period of time in which the body has voluntary control over whether to ingest it or not (after which the only controls are involuntary, such as vomiting or diarrhea).  Our sense of taste allows us to evaluate whether the material which has been put into the mouth is of potential use to the body (and should be swallowed) or not.

    amines, purines, and peptides (Fredriksson, 2003a).  An additional family which bind cAMP is not yet known in  humans (Bockaert, 1999).

Taste and vomeronasal receptors are not present in the most primitive chordates (Sherwood, 2005). In fish such as catfish, taste buds can actually occur over the entire surface of the body.


     There are four primary tastes that humans perceive.  The ability to detect sweet tastes is adaptive since it allows the body to identify foods which contain the potential energy stored in sugars.  Sensitivity to salt is important because it encourages the ingestion of foods which can replace the ions which may be lost through sweat.  Sour foods contain acids, perhaps because the food has been decomposed.  Such foods may contain bacterial toxins, potential parasites, etc. and sour tastes are perceived as unpleasant.  The ability of the human tongue to detect bitter compounds is far more sensitive than any of the other tastes.  Many of the compounds which are perceived as bitter are poisons if ingested in sufficient quantities.  Because of the unpleasant perception of these compounds, humans are unlikely to ingest sufficient quantities to be poisoned.  Such poisonous compounds are common in the natural world, given that plants commonly synthesize biologically harmful substances in their leaves as a deterrent to insects and herbivores.

     Taste receptors are G protein coupled receptors.  The T1Rs family of receptors is involved in the perception of sweet tastes.  Taste receptors TAS1R1 and TAS1R2 respond to a diversity of sweet compounds (sucrose, monosaccharides, artificial sweeteners, and the amino acids tryptophan and glycine) (Pin, 2003).  Many amino acids are perceived as sweet and stimulate receptors R1 and R3.   The following images are of taste receptors in taste buds.


TAS1R1 is responsible for umami taste, perceiving amino acids and monosodium glutamate (Pin, 2003).


TAS1R2 detects aspartane cyclamate and proteins which are very sweet.





The T2R family of taste receptors includes 80-120 T2 receptor genes (including pseudogenes which may represent 1/3 of these sequences) which are clustered in the genome and are responsible for our perception of bitter tastes (Adler, 2000).  Receptors 7, 8, 9, 10, 13, and 14 are located in a cluster on chromosome 12p13; receptors 3, 4, and 4 are located in a cluster on chromosome 7q31.  Gustatory cells can express multiple receptors and, as a result, a variety of toxic compounds with different chemical structures all produce the same bitter taste.  Even though there are a wide diversity of poisonous molecules to avoid ingesting, the body responds to all of them by regarding them all as similarly “bitter”. (Baringaga, 2000).













A recently discovered family of GPCR gustatory receptors in Drosophila.  The group seems to predate the origin of arthropods although there are some genes arranged in tandem arrays which appear to be of more recent origin. (Chyb, 2004).



     Olfactory receptors are the largest gene family in multicellular organisms and thus the largest gene family of the G-protein coupled receptors superfamily.  It is estimated that there are hundreds of these genes in the human genome (some estimate from 500 to 1000) and that olfactory receptors are capable of detecting millions of different compounds (Fuchs, 2001).  With about 500 genes, humans can detect more than 10,000 different odors and distinguish between 5,000 odors.  The only human system capable of distinguishing between a greater number of molecules is the immune system (Jones, 1998).

     Olfactory receptors may recognize multiple odorants and multiple olfactory receptors can recognize the same odorant (Adler, 2000; Halpern, 2003).  During primate evolution, many of these olfactory receptors have been inactivated.  In the olfactory epithelium, distinct sets of olfactory receptors are expressed in different areas.  Each olfactory neuron only expresses one allele of one receptor gene.  Each olfactory neuron expresses only one allele of one gene, although maternal and paternal alleles are both expressed throughout neuron populations (Lane, 2001). 

     The nematode C.elegans possesses many chemosensory receptors which are members of families unrelated to those in vertebrates and two additional families are known in Drosophila.  Thus, it appears that families of olfactory receptors have arisen several times (Lane, 2001).Lamprey olfactory receptor genes are the most primitive vertebrate olfactory receptors known. They seem to precede the genome duplication event and the subdivision of vertebrate olfactory genes into class I and class II genes (Freitag, 1999).

      One study identified 831 genes from 24 vertebrates.  There are two large groups of olfactory receptors designated as class I and class II.  With the exception of coelocanths, fish seem to only possess class I genes and a small number of them (100 genes in a catfish as opposed to several hundred genes in a mammal).  While most tetrapod genes are class II genes, many tetrapods (including humans) possess these class I genes as well.  Class II genes seem to have evolved as an adaptation to perceiving odorants in air rather than water. Of the class II genes, several subfamilies of one family have expanded considerably in mammals (Glusman, 2000) and one group has undergone expansion in primates (Fuchs, 2001).  Analysis of marsupial and monotreme olfactory receptors suggests that the first mammals had a very limited set, not too different from that of fish (Glusman, 2000).

     In teleost fish (such as the fish in the following photo), a limited number of ancestral genes appear to have duplicated to produce the diversity of olfactory genes which are specific to each lineage.  Although fish olfactory receptors in general are related in sequence and form a gene family, the olfactory receptors of an individual species can cluster in a gene family distinct from the gene families present in other species (Irie-Kushiyama, 2004).


     Olfactory receptor (OR) genes have no introns (except for one long intron in the 5’ untranslated region).  There are a number of subfamilies of OR genes and there are many which have clearly arisen through interchromosomal and intrachromosomal duplications.  There are clusters of olfactory genes in the genome; one cluster on human chromosome 17p13 possesses 17 OR genes (Lane, 2001). 

     There are differences in what humans can smell.  There are ethnic differences in the inability to smell musk and the inability to detect the sweaty odor of isovaleric acid.  There is an interesting variability in the detection of androstenone: half of those examined find that it has no odor (even when concentrated), 15% detect an odor but do not find it offensive (and may even find it pleasant), and 35% are very sensitive to its odor and find it unpleasant.  About two million Americans suffer from a loss or reduction of smell.  The olfactory system projects into the limbic system and odor-evoked memories are more emotional than those which are verbally cued.  Smell is involved in establishing the mother-infant bond (OMIM).

     There is evidence that olfactory receptor genes can be utilized by other body tissues as well.  Although the sequence of human PSGR suggests that it is an olfactory receptor and its mRNA is found in the olfactory epithelium, its protein is only known to be produced in the prostate.  In mice and rats, it can also be expressed in the brain, liver, and colon (Yuan, 2001).

      It was estimated that 48% of the olfactory receptor genes (388/802) in the human genome are functional.   Mice have fewer pseudogenes than humans: it is estimated that only about 20% of the 1,296-1,393 olfactory receptors are pseudogenes (Nimura, 2003).

Only about 27% of those in Old World monkeys and virtually none of those in New World monkeys are pseudogenes.    Zebrafish and mice also possess essentially no pseudogenes.  Two lemur species do have pseudogenes, and average of 37% (Rouquier, 2000; Zozulya, 2001).

     The nucleotide diversity of the coding regions of olfactory receptor genes ranges from 0 to 0.16% which is about twice as high as that observed in other coding regions and similar to that observed in noncoding regions of the genome.  One allele of OR17-31 C514T (with a frequency or 25%) is a pseudogene, containing a premature stop codon (Sharon, 2000).




     Amphibians, the first land vertebrates, had to adapt to perceiving odorants in air.

     Tetrapods typically have two anatomically distinct senses of smell: one is located on the olfactory epithelium covering the ethmoid bone and the other in the vomeronasal organ (VNO) at the base of the nasal septum.    Although this has long been considered a vestigial organ in humans, there is one human study has indicated that the VNO can be functional (Halpern, 2003).  A number of studies have suggested that the ancestors of Old World monkeys and apes experienced a mutation in the TRP2 gene which rendered the vomeronasal system nonfunctional and the vomeronasal receptors have gradually degenerated into nonfunctional pseudogenes since that event.  Thus humans develop structures two separate senses of smell although only one seems to be functional.

     It seems that the tetrapod vomeronasal system evolved from an olfactory region which was already present in fish, although not as a distinct structure.  Although goldfish do not have an anatomically distinct vomeronasal system as in tetrapods, it appears that the medial olfactory nerve, medial olfactory bulb, and the medial olfactory tract function in pheromone detection and are homologous to the vomeronasal system (VNS) of tetrapods while the lateral portions of these areas are homologous to the main olfactory system of tetrapods (Halpern, 2003; Cao, 1998).   Mammals typically possess about a hundred genes in each of the V1R and V2R vomeronasal receptor families. Bony fish are known to possess at least one member of each of these families (Hashiguchi, 2005).

     The vomeronasal organ’s primary function in many tetrapods is the detection of pheromones (although the olfactory epithelium can detect pheromones and the VNO may detect other odorants as well).  Humans synthesize and respond to pheromones (although which of the two olfactory systems is involved is not yet clear.  Axillary secretions from preovulatory women can shorten the menstrual cycle of other women (when applied to the upper lip) while secretions from the postovulatory phase can lengthen menstrual cycles.  Axillary secretions can affect sexual activity (Halpern, 2003).  In a number of mammals (including humans), different areas of the hypothalamus react to presumptive pheromones in males and females (Halpern, 2003).  The vomeronasal system in mice responds to substances in urine which vary by gender, strain, and hormonal status (Halpern, 2003). 

  There are two families of vomeronasal receptors: the V1R family includes an estimated 30-100 genes and the V2R family includes about 140 genes.  There seems to be a V3R family of about 100 genes (although some feel this should be considered a divergent subfamily of V1R) (Halpern, 2003). Fish possess homologs of both V1r and V2r pheromone receptors, although they lack a vomeronasal organ (Pfister, 2005).Vomeronasal neurons commonly express multiple receptor genes, unlike olfactory neurons. There are 2 distinct populations of VNO neurons (Halpern, 2003; Matsunami, 1997; Herrada, 1997).   Mice possess between 200 and 300 genes for two families of vomeronasal receptors.  Many of these vomeronasal genes have resulted from duplications dating from about the time of the separation of the mice and rat lineages.  (Lane, 2002). Mice and rats possess different numbers of functional V1R genes: 187 and 102, respectively (Grus, 2005).

     The VNO is well developed in reptiles and monotremes.  It is smaller but well developed in marsupials, insectivores, rodents, and New World monkeys. (Weichert, 1970; Jones, 1998).  Amplification of the number of V1R genes occurred independently in marsupials and rodents (Grus, 2005). While the vomeronasal organ in New World monkeys seems to be functional, its function may be less adaptive than is the case in most mammals.  This reduction of importance in New World monkeys is inferred from a relaxed selective pressure on the TRPC2 gene (given the divergence in sequences), reports of pseudogenes for VNO receptors in marmosets, and the lack of evidence specifying the function of the VNO in NW monkeys (Linman, 2003; Liman, 1999).  Higher primates have a highly developed ability to see in color and the vomeronasal organ is reduced to the point of being potentially nonfunctional.  Birds possess tetrachromatic vision and also lack vomeronasal organs (Zhang, 2003).  In megachiropteran bats, the vomeronasal organ is present in embryos when they are 14 mm in length but is absent afterwards. (Halpern, 2003). Mice and rats possess different numbers of functional V1R genes: 187 and 102, respectively (Grus, 2005).

     Instead of involving cyclic nucleotides (like G proteins), the vomeronasal system seems to involve an ion channel of the transient receptor potential family (TRP) whose members are known in fruit flies and nematodes.  The TRPC2 (TRP2) gene is only expressed in the VNO and is essential for the function of sensory neurons, being located on sensory microvilli.  The only genes known to function specifically in the VNS are the TRP2 and VNO receptor genes. These are pseudogenes (TRP2 and a large number of receptor genes) in humans and related primates.  The TRP2 gene in humans possesses both frameshift mutations and premature stop codons.  It also possesses premature stop codons in all other apes and Old World monkeys whose sequences are known.  One stop codon, in exon 13 of TRP2 seems to have been the original gene mutation which deactivated the gene and thus the entire vomeronasal system.  This mutations is shared by virtually all Old World monkeys and apes (except orangutans where a subsequent mutation has converted TGA to CGA).

      Once TRP2 became a pseudogene, there would no longer have been a selective pressure to maintain functional VNO receptors.  Statistically, the small number of VNO receptor genes which still have open reading frames in humans falls into the expected range of the number which would remain after about 35 million years of mutation.  Of the 5 remaining V1R genes in humans, V1RL5 and V1RL3 seem to be in the process of pseudogenization, given the high frequency of mutations which exist in current human populations.  No V2R genes exist as open reading frames in humans.  Humans also have at least one V3R gene which is expressed in the apical portion of the VNO. (Zhang, 2003; Giorgi, 2000; Rodriguez; Kouros-Mehr, 2001   ; Ryba, 1997; Lane, 2001). 



     Androstenol and androstenone are components of sweat that are probably derived from androgen hormones.  There is five times more androstenone in male axillary sweat than in female sweat.  Perhaps as a result, there is a sexual dimorphism in the microbes which inhabit the axilla (Cornebacteria dominate in males as opposed to Micrococcaceae in females).  Concentrations of androstenol in male urine is three times higher than in females.  Females typically perceive androstenol as attractive and it may increase arousal while they tend to be repelled by the odor of androstenone.  Given this, it is not known why males produce high quantities of androstenone (Hohl, 2001; Thornhill, 1999).  Women rate olfactory cues as more important than visual cues in mate selection and arousal.  Women’s greatest sensitivity to androstenol is during ovulation (Thornhill, 1999).

     The odor of vaginal copulins (short chain fatty acids) in monkeys is a stimulant for sex and human females synthesize the same copulins.  The perception of components of female axillary sweat allow females to allow their menstrual cycles to come in sync with each other.  Males can react differently to axillary sweat produced at different stages of the menstrual cycle (Hohl, 2001; Gangestad, 1998).

     Males in many mammal species (including humans) increase testosterone production in response to the presence of females. 

 (Hohl, 2001).  Exposure to male pheromones affect females in a number of ways.  This exposure can alter LH levels, mood, increase number of social contacts with men, and can cause irregular menstrual cycles to become more regular (Hohl, 2001).



     MHC molecules are an essential component of the immune system’s ability to distinguish “self” from “nonself”.  Apparently, these variable “self” molecules can also contribute to individual odor, although the mechanism through which this occurs is not known.       There is some evidence that MHC differences are a factor in determining the reaction to the sweat of other people.  Surveys have shown that odor is a more important determinant for human females than males (Herz, 2002). 

     Mice preferentially mate with individuals dissimilar MHC genes.  Mice can be trained to distinguish between urine samples whose donors differ only in MHC loci and untrained mice have been shown to discriminate between the odors of mice which differ only in the alleles of a classical MHC gene (dm2).  MHC genes are thus involved in odor (Penn, 1998). Thus, natural selection would have acted on MHC molecules in both their capacities to defend against pathogens and for their odor (Carroll, 2002).

     Women prefer the odor of dissimilar MHC men and the odors of these men are more likely to remind them of partners they have had in the past.  These preferences were not observed in women taking contraceptives (Wedekind, 1995).  MHC-disassortative mating preferences might increase the number of individuals which are heterozygous for genes in the immune system and thus enhance the ability to combat diverse microbes (Penn, 1999).  Some studies have indicated that humans (particularly women) prefer the body odor of those whose MHC complex differs from theirs  (Penn, 1999; Hohl, 2001; Gangestad, 1998).



     MHC molecules are expressed in vomeronasal neurons and there is interest in determining whether this allows the VNO to measure degrees of relatedness of potential mates as a potential mechanism to suppress inbreeding (Hegde, 2003).  Male mice preferentially mate with females with different MHC proteins and females preferentially nest with females with similar MHC proteins (Beauchamp, 2000).  In mice, fetal MHC proteins produce odors that can be detected in maternal urine.  Male mice can distinguish between, and react to, the odor in maternal urine, showing a preference for females whose fetuses carried MHC proteins differing from those of the male (Beauchamp, 2000).  Females prefer urine of uninfected males to that of infected males (Ehman, 2001).  Untrained mice can distinguish between individuals which differ in some but not all MHC genes (Carroll, 2002).   Humans can also distinguish between the odors of mouse strains which differ only in their MHC (Wedekind, 1995).

      In rodents, females spontaneously abort same MHC embryos more frequently and in humans, the in vitro fertilization of same-MHC  embryos are more likely to fail  (Penn, 1999).  Studies among an inbred group of humans indicated that couples which share an MHC haplotype have longer than normal interbirth intervals and that there were fewer marriages between same-haplotype individuals than would be expected by chance  (Penn, 1999).



     While all males would have an advantage in producing an attractive scent, females have an advantage in detecting “honest signaling from males to evaluate them in mate selection (Thornhill, 1999). 

      The deviation from perfect symmetry, termed fluctuating symmetry, has been correlated with a man’s number of sexual partners, the number of extrapair partners, and even the number of their partner’s orgasms (Gangestad, 1998).  Fluctuating asymmetry (FA) can be influenced by mutations, inbreeding, and homozygosity.  Low FA increased probability of lower physical and mental health.  The bacteria which colonize skin may be related to health.  (Thornhill, 1999).

     Female desire changes over the course of the menstrual cycle, with the greatest number of extra-pair couplings occurring around the midpoint of the menstrual cycle.  Women prefer the scent of men with a greater degree of symmetry than less symmetrical men in the midpoint of the menstrual cycle.  These olfactory preferences are not observed at other points of the menstrual cycle or in women taking contraceptives (Gangestad, 1998).  Ovulating women prefer the odor of more symmetrical men although this is not observed in women on contraceptives or men’s preferences for women (Thornhill, 1999).

     Many perfume components in use today were used by humans living five thousand years ago in areas such as China, India, and Egypt.  Analyses have indicated that perfume preferences vary with an individual’s MHC alleles (Milinski, 2001).