Figure 7 | Scientific Reports

Figure 7

From: The Bitter Taste Receptor TAS2R16 Achieves High Specificity and Accommodates Diverse Glycoside Ligands by using a Two-faced Binding Pocket

Figure 7

The N96T probenecid-resistance mutation decreases the EC50 for TAS2R16 activation. (a) Alignment of partial TAS2R16 sequences (corresponding to residues 89–100 in human TAS2R16) demonstrates that N96 (red highlight) replaced T96 during primate evolution. Shown are TAS2R16 sequences from Gorilla gorilla (western gorilla), Pan troglodytes (chimpanzee), Papio anubis (olive baboon), Pongo pygmaeus (Bornean orangutan), Macaca mulatta (rhesus macaque), Trachypithecus cristatus (silvery lutung), Sapajus paella (tufted capuchin monkey), Callithrix jacchus (marmoset), Nycticebus coucang (Sunda slow loris), Lemur catta (ring-tailed lemur), Bos bovis (cow), Loxodonta africana (African elephant), Cavia porcellus (guinea pig), Cricetulus griseus (Chinese hamster), Equus caballus (horse), Mus musculus (mouse), Rattus norvegicus (rat), and Sus scrofa (pig). Dose-response studies were performed for wild-type (WT), N96T, and N96A variants of TAS2R16 using ligands (b) salicin or (c) 4-NP-β-mannoside. Dose-response curves for salicin and 4-NP-β-mannoside with wild-type TAS2R16, and N96T and N96A variants demonstrated that N96T resulted in a greater than 5-fold decrease in EC50 for both compounds relative to wild-type TAS2R16. Error bars represent the standard deviation, n = 4–8 replicate points.