taste is salty na+, sodium, molecules pass through the na+ channels. depolarization takes place ii. part ii is the transduction pathway of the relay molecules.2. cation, such as k+, channels are opened. iii. part iii is the response of the cell. 3. an influx of ca+ ions is activated.4. the ca+ activates neurotransmitters. 5. a signal is sent to the neuron attached to the taste bud. salt various receptors have also been proposed for salty tastes, along with the possible taste detection of lipids, complex carbohydrates, and water. evidence for these receptors had been unconvincing in most mammal studies. for example, the proposed enac receptor for sodium detection can only be shown to contribute to sodium taste in drosophila. however, proteolyzed forms of enac have been shown to function as a human salt taste receptor. proteolysis is the process where a protein is cleaved. the mature form of enac is thought to be proteolyzed, however the characterization of which proteolyzed forms exist in which tissues is incomplete. proteolysis of cells created to overexpress hetermulitmeric enac comprising alpha, beta and gamma subunits was used to identify compounds that selectively enhanced the activity of proteolyzed enac versus non-proteolyzed enac. human sensory studies demonstrated that a compound that enhances proteolyzed enac functions to enhance the salty taste of table salt, or sodium chloride, confirming proteolyzed enac as the first human salt taste receptor. carbonation an enzyme connected to the sour receptor transmits information about carbonated water. fat a possible taste receptor for fat, cd36, has been identified. cd36 has been localized to the circumvallate and foliate papillae, which are present in taste buds and where lingual lipase is produced, and research has shown that the cd36 receptor binds long chain fatty acids. differences in the amount of cd36 expression in human subjects was associated with their ability to taste fats, creating a case for the receptor's relationship to fat tasting. further research into the cd36 receptor could be useful in determining the existence of a true fat-tasting receptor. gpr120 and 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. types human bitter taste receptor genes are named tas2r1 to tas2r64, with many gaps due to non-existent genes, pseudogenes or proposed genes that have not been annotated to the most recent human genome assembly. many bitter taste receptor genes also have confusing synonym names with several different gene names referring to the same gene. see table below for full list of human bitter taste receptor genes: class gene synonyms aliases locus description type 1(sweet) tas1r1 gpr70 1p36.23 tas1r2 gpr71 1p36.23 tas1r3 1p36 type 2(bitter) tas2r1 5p15 tas2r2 7p21.3 pseudogene tas2r3 7q31.3-q32 tas2r4 7q31.3-q32 tas2r5 7q31.3-q32 tas2r6 7 not annotated in human genome assembly tas2r7 12p13 tas2r8 12p13 tas2r9 12p13 tas2r10 12p13 tas2r11 absent in humans tas2r12 tas2r26 12p13.2 pseudogene tas2r13 12p13 tas2r14 12p13 tas2r15 12p13.2 pseudogene tas2r16 7q31.1-q31.3 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 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 tas2r39 7q34 tas2r40 gpr60 7q34 tas2r41 7q34 tas2r42 12p13 tas2r43 12p13.2 tas2r45 gpr59 12 tas2r46 12p13.2 tas2r50 tas2r51 12p13.2 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 loss of function in many species, taste receptors have shown loss of functions. the evolutionary process in which taste receptors lost their function is believed to be an adaptive evolution where it is associated with feeding ecology to drive specialization and bifurcation of taste receptors. out of all the taste receptors, bitter, sweet, and umami are shown to have a correlation between inactivation of taste receptors and feeding behavior. however, there are no strong evidences that support any vertebrates are missing the bitter taste receptor genes. 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 pseudogenization 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.