Journal articles: 'Taste gene'

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Fernández-Carrión, Rebeca, Jose V. Sorlí, Oscar Coltell, Eva C. Pascual, Carolina Ortega-Azorín, Rocío Barragán, Ignacio M. Giménez-Alba, et al. "Sweet Taste Preference: Relationships with Other Tastes, Liking for Sugary Foods and Exploratory Genome-Wide Association Analysis in Subjects with Metabolic Syndrome." Biomedicines 10, no. 1 (December 31, 2021): 79. http://dx.doi.org/10.3390/biomedicines10010079.

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Taste perception and its association with nutrition and related diseases (type 2 diabetes, obesity, metabolic syndrome, cardiovascular, etc.) are emerging fields of biomedicine. There is currently great interest in investigating the environmental and genetic factors that influence sweet taste and sugary food preferences for personalized nutrition. Our aims were: (1) to carry out an integrated analysis of the influence of sweet taste preference (both in isolation and in the context of other tastes) on the preference for sugary foods and its modulation by type 2 diabetes status; (2) as well as to explore new genetic factors associated with sweet taste preference. We studied 425 elderly white European subjects with metabolic syndrome and analyzed taste preference, taste perception, sugary-foods liking, biochemical and genetic markers. We found that type 2 diabetic subjects (38%) have a small, but statistically higher preference for sweet taste (p = 0.021) than non-diabetic subjects. No statistically significant differences (p > 0.05) in preferences for the other tastes (bitter, salty, sour or umami) were detected. For taste perception, type 2 diabetic subjects have a slightly lower perception of all tastes (p = 0.026 for the combined “total taste score”), bitter taste being statistically lower (p = 0.023). We also carried out a principal component analysis (PCA), to identify latent variables related to preferences for the five tastes. We identified two factors with eigenvalues >1. Factor 2 was the one with the highest correlation with sweet taste preference. Sweet taste preference was strongly associated with a liking for sugary foods. In the exploratory SNP-based genome-wide association study (GWAS), we identified some SNPs associated with sweet taste preference, both at the suggestive and at the genome-wide level, especially a lead SNP in the PTPRN2 (Protein Tyrosine Phosphatase Receptor Type N2) gene, whose minor allele was associated with a lower sweet taste preference. The PTPRN2 gene was also a top-ranked gene obtained in the gene-based exploratory GWAS analysis. In conclusion, sweet taste preference was strongly associated with sugary food liking in this population. Our exploratory GWAS identified an interesting candidate gene related with sweet taste preference, but more studies in other populations are required for personalized nutrition.

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Feeney, E., S. O'Brien, A. Scannell, A. Markey, and E. R. Gibney. "Genetic variation in taste perception: does it have a role in healthy eating?" Proceedings of the Nutrition Society 70, no. 1 (November 22, 2010): 135–43. http://dx.doi.org/10.1017/s0029665110003976.

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Taste is often cited as the factor of greatest significance in food choice, and has been described as the body's ‘nutritional gatekeeper’. Variation in taste receptor genes can give rise to differential perception of sweet, umami and bitter tastes, whereas less is known about the genetics of sour and salty taste. Over twenty-five bitter taste receptor genes exist, of which TAS2R38 is one of the most studied. This gene is broadly tuned to the perception of the bitter-tasting thiourea compounds, which are found in brassica vegetables and other foods with purported health benefits, such as green tea and soya. Variations in this gene contribute to three thiourea taster groups of people: supertasters, medium tasters and nontasters. Differences in taster status have been linked to body weight, alcoholism, preferences for sugar and fat levels in food and fruit and vegetable preferences. However, genetic predispositions to food preferences may be outweighed by environmental influences, and few studies have examined both. The Tastebuddies study aimed at taking a holistic approach, examining both genetic and environmental factors in children and adults. Taster status, age and gender were the most significant influences in food preferences, whereas genotype was less important. Taster perception was associated with BMI in women; nontasters had a higher mean BMI than medium tasters or supertasters. Nutrient intakes were influenced by both phenotype and genotype for the whole group, and in women, the AVI variation of the TAS2R38 gene was associated with a nutrient intake pattern indicative of healthy eating.

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Williams, Derek. "Good taste gene." New Scientist 216, no. 2896-2897 (December 2012): 41. http://dx.doi.org/10.1016/s0262-4079(12)63259-x.

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Lalueza-Fox, Carles, Elena Gigli, Marco de la Rasilla, Javier Fortea, and Antonio Rosas. "Bitter taste perception in Neanderthals through the analysis of the TAS2R38 gene." Biology Letters 5, no. 6 (August 12, 2009): 809–11. http://dx.doi.org/10.1098/rsbl.2009.0532.

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The bitter taste perception (associated with the ability or inability to taste phenylthiocarbamide) is mediated by the TAS2R38 gene. Most of the variation in this gene is explained by three common amino-acid polymorphisms at positions 49 (encoding proline or alanine), 262 (alanine or valine) and 296 (valine or isoleucine) that determine two common isoforms: proline–alanine–valine (PAV) and alanine–valine–isoleucine (AVI). PAV is the major taster haplotype (heterozygote and homozygote) and AVI is the major non-taster haplotype (homozygote). Amino acid 49 has the major effect on the distinction between tasters and non-tasters of all three variants. The sense of bitter taste protects us from ingesting toxic substances, present in some vegetables, that can affect the thyroid when ingested in large quantities. Balancing selection has been used to explain the current high non-taster frequency, by maintaining divergent TAS2R38 alleles in humans. We have amplified and sequenced the TAS2R38 amino acid 49 in the virtually uncontaminated Neanderthal sample of El Sidrón 1253 and have determined that it was heterozygous. Thus, this Neanderthal was a taster individual, although probably slightly less than a PAV homozygote. This indicates that variation in bitter taste perception pre-dates the divergence of the lineages leading to Neanderthals and modern humans.

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Hirai, Ryoji, and Minoru Ikeda. "Bitter Taste Receptor Gene in Patients with Taste Disorders." Otolaryngology–Head and Neck Surgery 145, no. 2_suppl (August 2011): P147. http://dx.doi.org/10.1177/0194599811415823a41.

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Lush, Ian E., and Gail Holland. "The genetics of tasting in mice: V. Glycine and cycloheximide." Genetical Research 52, no. 3 (December 1988): 207–12. http://dx.doi.org/10.1017/s0016672300027671.

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SummaryGlycine tastes both bitter and sweet to mice but there are differences between strains in their ability to detect each taste. With respect to the bitter taste, fifteen strains were classified as tasters and twelve strains as non-tasters. The difference is due to a single gene, Glb (glycine bitterness). Cycloheximide tastes bitter to all mice at a concentration of 8 μM, but strain differences in sensitivity to the taste of cycloheximide can be detected at lower concentrations. The BXD RI strains can be classified into two groups with respect to sensitivity to cycloheximide. This is probably due to the segregation of two alleles of a single gene, Cyx. A comparison of the distribution in RI strains of alleles of four bitterness-tasting genes shows that the loci are all closely linked and are probably in the order Cyx–Qui–Rua–Glb.

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Montmayeur, Jean-Pierre, Stephen D. Liberles, Hiroaki Matsunami, and Linda B. Buck. "A candidate taste receptor gene near a sweet taste locus." Nature Neuroscience 4, no. 5 (May 2001): 492–98. http://dx.doi.org/10.1038/87440.

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Tordoff, Michael G., and Hillary T. Ellis. "Taste dysfunction in BTBR mice due to a mutation of Itpr3, the inositol triphosphate receptor 3 gene." Physiological Genomics 45, no. 18 (September 15, 2013): 834–55. http://dx.doi.org/10.1152/physiolgenomics.00092.2013.

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The BTBR T+ tf/J (BTBR) mouse strain is indifferent to exemplars of sweet, Polycose, umami, bitter, and calcium tastes, which share in common transduction by G protein-coupled receptors (GPCRs). To investigate the genetic basis for this taste dysfunction, we screened 610 BTBR × NZW/LacJ F2 hybrids, identified a potent QTL on chromosome 17, and isolated this in a congenic strain. Mice carrying the BTBR/BTBR haplotype in the 0.8-Mb (21-gene) congenic region were indifferent to sweet, Polycose, umami, bitter, and calcium tastes. To assess the contribution of a likely causative culprit, Itpr3, the inositol triphosphate receptor 3 gene, we produced and tested Itpr3 knockout mice. These were also indifferent to GPCR-mediated taste compounds. Sequencing the BTBR form of Itpr3 revealed a unique 12 bp deletion in Exon 23 (Chr 17: 27238069; Build 37). We conclude that a spontaneous mutation of Itpr3 in a progenitor of the BTBR strain produced a heretofore unrecognized dysfunction of GPCR-mediated taste transduction.

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Kang, Byung-Jun, Jin-Woo Park, Sang-Yen Geum, Un-Kyung Kim, Seung-Heon Shin, and Mi-Kyung Ye. "Role of the TAS2R38 Bitter Taste Receptor Gene Single Nucleotide Polymorphism in Patients With Taste Disorders." Korean Journal of Otorhinolaryngology-Head and Neck Surgery 64, no. 11 (November 21, 2021): 800–805. http://dx.doi.org/10.3342/kjorl-hns.2021.00486.

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Background and Objectives Several studies have shown that three single nucleotide polymorphisms (SNPs) in the TAS2R38 gene demonstrate a strong association with the ability to sense the bitter taste of phenylthiocarbamide (PTC) in. We have previously reported about TAS2R38 genotypes in normal volunteers. The aim of this study was to investigate the role TAS2R38 gene plays in taste disorder by examining SNPs in the TAS2R38 gene in taste disorder patients.Subjects and Method Ninety-four patients with taste dysfunction from multiple etiologies were enrolled. The genotypes were defined by identifying SNPs on the TAS2R38 gene. The proportion of different TAS2R38 genotypes in the group was compared with that in the normal volunteers of our previous study. The whole mouth taste threshold tests were performed and the thresholds were compared among the three different genotypic groups.Results The proportion of each diplotype in taste disorder patients were as follows: PAV/ PAV 36.2% (34/94), PAV/AVI 34.0% (32/94), and AVI/AVI 29.8% (28/94). The proportion of AVI/AVI type was higher in the group than in the normal volunteers (p=0.031). The detection and recognition thresholds of all four basic tastes were increased in the order of PAV/PAV, PAV/AVI, and AVI/AVI genotypes.Conclusion The proportion of AVI/AVI homozygous was significantly higher in taste disorder patients than in the normal volunteers. Our findings suggest that the genotypes of TAS2R38 may represent one of the risk factors responsible for the development of taste disorders.

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Isono, Kunio, Kohei Ueno, Masayuki Ohta, and Hiromi Morita. "Drosophila sweet taste receptor." Pure and Applied Chemistry 74, no. 7 (January 1, 2002): 1159–65. http://dx.doi.org/10.1351/pac200274071159.

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Like the Sac locus controlling sugar sensitivity in mice, the taste gene Tre of the fruitfly Drosophila was discovered in wild populations as a genetic dimorphism controlling gustatory sensitivity to a sugar trehalose. By activating a P-element transposon near the gene locus we obtained induced Tre mutations and analyzed the associated changes in gene organizations and the mRNA expressions. The analysis showed that Tre is identical to Gr5a, a gene that belongs to a novel seven-transmembrane receptor family expressed in chemosensory neurons and predicted to encode chemosensory receptors. Thus, Gr5a is a candidate sweet taste receptor in the fly. An amino acid substitution in the second intracellular loop domain was identified to be functionally correlated with the genetic dimorphism of Tre. Since Tre controls sweet taste sensitivity to a limited subset of sugars, other Gr genes phylogenetically related to Tre may also encode sweet taste receptors. Those candidate sweet taste receptors, however, are phylogenetically distinct from vertebrate sweet taste receptors, suggesting that the sweet taste receptors in animals do not share a common origin.

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Chamoun, Elie, Nicholas Carroll, Lisa Duizer, Wenjuan Qi, Zeny Feng, Gerarda Darlington, Alison Duncan, Jess Haines, and David Ma. "The Relationship between Single Nucleotide Polymorphisms in Taste Receptor Genes, Taste Function and Dietary Intake in Preschool-Aged Children and Adults in the Guelph Family Health Study." Nutrients 10, no. 8 (July 29, 2018): 990. http://dx.doi.org/10.3390/nu10080990.

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Taste is a fundamental determinant of food selection, and inter-individual variations in taste perception may be important risk factors for poor eating habits and obesity. Characterizing differences in taste perception and their influences on dietary intake may lead to an improved understanding of obesity risk and a potential to develop personalized nutrition recommendations. This study explored associations between 93 single nucleotide polymorphisms (SNPs) in sweet, fat, bitter, salt, sour, and umami taste receptors and psychophysical measures of taste. Forty-four families from the Guelph Family Health Study participated, including 60 children and 65 adults. Saliva was collected for genetic analysis and parents completed a three-day food record for their children. Parents underwent a test for suprathreshold sensitivity (ST) and taste preference (PR) for sweet, fat, salt, umami, and sour as well as a phenylthiocarbamide (PTC) taste status test. Children underwent PR tests and a PTC taste status test. Analysis of SNPs and psychophysical measures of taste yielded 23 significant associations in parents and 11 in children. After adjusting for multiple hypothesis testing, the rs713598 in the TAS2R38 bitter taste receptor gene and rs236514 in the KCNJ2 sour taste-associated gene remained significantly associated with PTC ST and sour PR in parents, respectively. In children, rs173135 in KCNJ2 and rs4790522 in the TRPV1 salt taste-associated gene remained significantly associated with sour and salt taste PRs, respectively. A multiple trait analysis of PR and nutrient composition of diet in the children revealed that rs9701796 in the TAS1R2 sweet taste receptor gene was associated with both sweet PR and percent energy from added sugar in the diet. These findings provide evidence that for bitter, sour, salt, and sweet taste, certain genetic variants are associated with taste function and may be implicated in eating patterns. (Support was provided by the Ontario Ministry of Agriculture, Food, and Rural Affairs).

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Wang, Yupeng, Ying Sun, and Paule Valery Joseph. "Contrasting Patterns of Gene Duplication, Relocation, and Selection Among Human Taste Genes." Evolutionary Bioinformatics 17 (January 2021): 117693432110351. http://dx.doi.org/10.1177/11769343211035141.

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In humans, taste genes are responsible for perceiving at least 5 different taste qualities. Human taste genes’ evolutionary mechanisms need to be explored. We compiled a list of 69 human taste-related genes and divided them into 7 functional groups. We carried out comparative genomic and evolutionary analyses for these taste genes based on 8 vertebrate species. We found that relative to other groups of human taste genes, human TAS2R genes have a higher proportion of tandem duplicates, suggesting that tandem duplications have contributed significantly to the expansion of the human TAS2R gene family. Human TAS2R genes tend to have fewer collinear genes in outgroup species and evolve faster, suggesting that human TAS2R genes have experienced more gene relocations. Moreover, human TAS2R genes tend to be under more relaxed purifying selection than other genes. Our study sheds new insights into diverse and contrasting evolutionary patterns among human taste genes.

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UGAWA, Shinya, and Shoichi SHIMADA. "Genes for Taste Receptors. Isolation of a Gene for a Sour Taste Receptor." Seibutsu Butsuri 40, no. 2 (2000): 105–10. http://dx.doi.org/10.2142/biophys.40.105.

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Li, X., A. A. Bachmanov, K. Maehashi, W. Li, R. Lim, J. G. Brand, G. K. Beauchamp, D. R. Reed, C. Thai, and W. B. Floriano. "Sweet Taste Receptor Gene Variation and Aspartame Taste in Primates and Other Species." Chemical Senses 36, no. 5 (March 16, 2011): 453–75. http://dx.doi.org/10.1093/chemse/bjq145.

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Huang, A. Y., and S. Y. Wu. "Calcitonin Gene-Related Peptide Reduces Taste-Evoked ATP Secretion from Mouse Taste Buds." Journal of Neuroscience 35, no. 37 (September 16, 2015): 12714–24. http://dx.doi.org/10.1523/jneurosci.0100-15.2015.

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Sandell, Mari A., and Paul A. S. Breslin. "Variability in a taste-receptor gene determines whether we taste toxins in food." Current Biology 16, no. 18 (September 2006): R792—R794. http://dx.doi.org/10.1016/j.cub.2006.08.049.

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Lush, I. E., N. Hornigold, P. King, and J. P. Stoye. "The genetics of tasting in mice VII. Glycine revisited, and the chromosomal location of Sac and Soa." Genetical Research 66, no. 2 (October 1995): 167–74. http://dx.doi.org/10.1017/s0016672300034510.

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SummaryPrevious work which appeared to show that some strains of mice taste glycine solutions as bitter has been found to be in error. The bitterness came from copper glycinate which formed in the brass drinking spouts. Taste testing with copper glycinate shows that the genetical data identifying the gene Glb are still valid. The close linkage of Glb and Rua has been confirmed. Most strains of mice prefer glycine solution to water, presumably because the glycine tastes sweet. The degree of preference for glycine is correlated with the degree of preference for other sweet substances such as saccharin or acesulfame. The gene dpa appears not to be involved.The sweetness tasting gene Sac has been mapped to chromosome 4 at 8·1 ± 3·4 cM distal to Nppa (formerly Pnd). The bitterness tasting gene Soa is very closely linked to Prp on chromosome 6 (no recombinants among 67 backcross progeny). It is suggested that the sweetness and bitterness tasting genes have descended from a common ancestral tasting gene which existed before the tetraploidization of the genome which took place in early vertebrate evolution.

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Henslee, Dillan, Melinda Ellison, Brenda Murdoch, J. Bret Taylor, and Joel Yelich. "PSIV-20 TAS2R genes in sheep and cattle compared to humans." Journal of Animal Science 97, Supplement_3 (December 2019): 229–30. http://dx.doi.org/10.1093/jas/skz258.467.

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Abstract The taste receptor gene family has been extensively studied in human and some genes have been linked to food preferences and addiction; however, research in foraging ruminants is limited. Identification of taste receptor genes in the sheep genome may provide insight regarding individual dietary range plant preferences. Bitter taste has been a large focus of research since Arthur Fox accidentally discovered the bitter tasting compound phenylthiocarbamide (PTC) and observed that bitter taste perception in humans is a variable trait. In theory, individuals who are sensitive to bitter taste will likely consume less bitter tasting foods, which are often antioxidant rich, and be more prone to disease and illness. The objective of this study was to examine known taste receptor genes in sheep and cattle and compare them with humans to determine similarities and differences. Type 2 taste receptors (T2R’s) are the only receptor of the taste gene family to perceive bitterness in foods. Using NCBI genome data viewer, the taste genes were identified on the human (GRCh38.p12), cattle (ARS-UCD1.2), and sheep (Oar_4.0; OORI1) genomes. All 3 species have one T2R gene cluster in common, which includes T2R genes 3, 4, 5, 38, 39, 40, 60, and 41. The span of this cluster is similar for humans (1,457,940 bp), sheep (1,541,593 bp), and cattle (1,594,610 bp). One gene in particular (T2R38) has been associated with PTC sensitivity and linked to aversion of some bitter tasting food in humans. Previous research on T2R38 identified 5 haplotypes, each expressing aversion to bitter taste differently. There is another T2R gene cluster which contains 10 annotated genes in sheep and cattle genomes; however, this region contains an additional 10 genes annotated in the human genome. Understanding genetic variation in TAS2R genes may translate to dietary preferences of sheep grazing on rangelands.

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Lee, Gyu-Ho, Byung-Wook Yun, and Kyung-Min Kim. "Analysis of QTLs Associated with the Rice Quality Related Gene by Double Haploid Populations." International Journal of Genomics 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/781832.

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We investigated the growth characteristics and analyzed the physicochemical properties of a doubled haploid population derived from a cross between “Cheongcheong” and “Nagdong” to breed a rice variety that tastes good after cooking and to detect quantitative trait loci (QTLs) associated with the taste of cooked rice. The results showed that these compounds also represent a normal distribution. Correlation analysis of the amylose, protein, and lipid contents indicated that each compound is related to the taste of cooked rice. The QTLs related to amylose content were 4 QTLs, protein content was 2 QTLs, and lipid content was 2 QTLs. Four of the QTLs associated with amylose content were detected on chromosomes 7 and 11. The index of coincidence for the QTLs related to amylose, protein, and lipid content was 70%, respectively. These markers showing high percentage of coincidence can be useful to select desirable lines for rice breeding.

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Angotzi, Anna Rita, Sara Puchol, Jose M. Cerdá-Reverter, and Sofia Morais. "Insights into the Function and Evolution of Taste 1 Receptor Gene Family in the Carnivore Fish Gilthead Seabream (Sparus aurata)." International Journal of Molecular Sciences 21, no. 20 (October 19, 2020): 7732. http://dx.doi.org/10.3390/ijms21207732.

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A plethora of molecular and functional studies in tetrapods has led to the discovery of multiple taste 1 receptor (T1R) genes encoding G-protein coupled receptors (GPCRs) responsible for sweet (T1R2 + T1R3) and umami (T1R1 + T1R3) taste. In fish, the T1R gene family repertoires greatly expanded because of several T1R2 gene duplications, and recent studies have shown T1R2 functional divergence from canonical mammalian sweet taste perceptions, putatively as an adaptive mechanism to develop distinct feeding strategies in highly diverse aquatic habitats. We addressed this question in the carnivore fish gilthead seabream (Sparus aurata), a model species of aquaculture interest, and found that the saT1R gene repertoire consists of eight members including saT1R1, saT1R3 and six saT1R2a-f gene duplicates, adding further evidence to the evolutionary complexity of fishT1Rs families. To analyze saT1R taste functions, we first developed a stable gene reporter system based on Ca2+-dependent calcineurin/NFAT signaling to examine specifically in vitro the responses of a subset of saT1R heterodimers to L-amino acids (L-AAs) and sweet ligands. We show that although differentially tuned in sensitivity and magnitude of responses, saT1R1/R3, saT1R2a/R3 and saT1R2b/R3 may equally serve to transduce amino acid taste sensations. Furthermore, we present preliminary information on the potential involvement of the Gi protein alpha subunits saGαi1 and saGαi2 in taste signal transduction.

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Abaturov, Aleksandr, Anna Nikulina, and Dmitriy Nikulin. "TAS2R38 taste receptor gene and metabolically unhealthy obesity." Metabolism 128 (March 2022): 155003. http://dx.doi.org/10.1016/j.metabol.2021.155003.

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Medler, Kathryn F., Anne Hansen, and Richard C. Bruch. "Odorant receptor gene expression in catfish taste tissue." NeuroReport 9, no. 18 (December 1998): 4103–7. http://dx.doi.org/10.1097/00001756-199812210-00018.

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Boughter, John D., and Glayde Whitney. "Behavioral Specificity of the Bitter Taste Gene Soa." Physiology & Behavior 63, no. 1 (December 1997): 101–8. http://dx.doi.org/10.1016/s0031-9384(97)00398-3.

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Ftuwi, Habtom, Rheinallt Parri, and Afzal R. Mohammed. "Novel, Fully Characterised Bovine Taste Bud Cells of Fungiform Papillae." Cells 10, no. 9 (September 2, 2021): 2285. http://dx.doi.org/10.3390/cells10092285.

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Current understanding of functional characteristics and biochemical pathways in taste bud cells have been hindered due the lack of long-term cultured cells. To address this, we developed a holistic approach to fully characterise long term cultured bovine taste bud cells (BTBCs). Initially, cultured BTBCs were characterised using RT-PCR gene expression profiling, immunocytochemistry, flowcytometry and calcium imaging, that confirmed the cells were mature TBCs that express taste receptor genes, taste specific protein markers and capable of responding to taste stimuli, i.e., denatonium (2 mM) and quinine (462.30 μM). Gene expression analysis of forty-two genes implicated in taste transduction pathway (map04742) using custom-made RT-qPCR array revealed high and low expressed genes in BTBCs. Preliminary datamining and bioinformatics demonstrated that the bovine α-gustducin, gustatory G-protein, have higher sequence similarity to the human orthologue compared to rodents. Therefore, results from this work will replace animal experimentation and provide surrogate cell-based throughput system to study human taste transduction.

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Lush, Ian E. "The genetics of tasting in mice: IV. The acetates of raffinose, galactose and β-lactose." Genetical Research 47, no. 2 (April 1986): 117–23. http://dx.doi.org/10.1017/s0016672300022941.

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SUMMARYThirty strains of mice were tested for their ability to taste a 0·4 mM solution of raffinose undecaacetate (RUA). There were large strain differences. Some strains showed little or no ability to taste the RUA. Two strains, SWR and Schneider, could taste RUA because they possess the Soaa allele which enables them to taste a variety of acetylated monosaccharides. Three other strains, BALB/c, DBA/2 and C3H, could taste RUA because they possess the Ruaa allele which enables them to taste some larger structure which is a feature of the molecule as a whole. The gene Rua is tightly linked to the gene for quinine tasting. Qui, but the distribution of their alleles among the strains shows that they are different genes. It is suggested that there is in the mouse a cluster of tightly-linked genes, each one determining a taste receptor for a different bitter substance or chemical group. The relevance of these findings to the physiology of tasting is discussed.

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Ergün, Can, and Meral Aksoy. "Relationships between the hTAS2R38 genotype, food choice, and anthropometric variables in normal-weighted and overweight adults." Genetika 45, no. 2 (2013): 381–91. http://dx.doi.org/10.2298/gensr1302381e.

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Aim: Taste is a major determinant of food choice; however, there is a great lack of knowledge about how taste perception affects human nutrition. Bitter taste perception presents unique opportunities for investigating this subject. The aim of this study was to determine whether polymorphisms on the bitter taste receptor gene hTAS2R38 affect an individual?s food choices and some anthropometric variables. Subjects and Method: In this study, the possible relationship between food preferences, body weight, and polymorphisms on hTAS2R38 was investigated in healthy volunteers (n=178) who weighed within the normal range (BMI: 20-24.9 kg/m2, n=90) and those who were overweight, but otherwise healthy (BMI ? 25.0 kg/m2, n=88). Descriptive information about the subjects was collected via a questionnaire, and anthropometric measurements were taken by the researcher. Records of three consecutive days of food consumption were collected to determine each subject?s macronutrient intake. For identification of the hTAS2R38 genotype, samples were taken from each participant's in-mouth epithelial cell line, and the genetic material was analyzed at the laboratory for Rs713598. Results: The percentage of ?non-tasters? (n=42) among the whole population was 23.6% (C-Homozygote: 23.6%) while ?tasters? (n=136) comprised 76.4% (CG-Heterozygote: 46.6%, G-Homozygote: 29.8%). When group-wide and between-group comparisons were made, it was revealed that taster status didn?t affect differences in anthropometric measures. Detected differences in macronutrient intake were due to gender. Discussion: Polymorphisms on hTAS2R38 bitter taste receptor gene had no effect on variables such as body weight, anthropometric variables, body fat percentage, or food choices within the study population.

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Chaudhari, Nirupa, and Stephen D. Roper. "The cell biology of taste." Journal of Cell Biology 190, no. 3 (August 9, 2010): 285–96. http://dx.doi.org/10.1083/jcb.201003144.

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Taste buds are aggregates of 50–100 polarized neuroepithelial cells that detect nutrients and other compounds. Combined analyses of gene expression and cellular function reveal an elegant cellular organization within the taste bud. This review discusses the functional classes of taste cells, their cell biology, and current thinking on how taste information is transmitted to the brain.

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Risso, Davide, Eduardo Sainz, Gabriella Morini, Sergio Tofanelli, and Dennis Drayna. "Taste Perception of Antidesma bunius Fruit and Its Relationships to Bitter Taste Receptor Gene Haplotypes." Chemical Senses 43, no. 7 (June 7, 2018): 463–68. http://dx.doi.org/10.1093/chemse/bjy037.

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Inoue, Masashi, John I. Glendinning, Maria L. Theodorides, Sarah Harkness, Xia Li, Natalia Bosak, Gary K. Beauchamp, and Alexander A. Bachmanov. "Allelic variation of the Tas1r3 taste receptor gene selectively affects taste responses to sweeteners: evidence from 129.B6-Tas1r3 congenic mice." Physiological Genomics 32, no. 1 (December 2007): 82–94. http://dx.doi.org/10.1152/physiolgenomics.00161.2007.

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The Tas1r3 gene encodes the T1R3 receptor protein, which is involved in sweet taste transduction. To characterize ligand specificity of the T1R3 receptor and the genetic architecture of sweet taste responsiveness, we analyzed taste responses of 129.B6- Tas1r3 congenic mice to a variety of chemically diverse sweeteners and glucose polymers with three different measures: consumption in 48-h two-bottle preference tests, initial licking responses, and responses of the chorda tympani nerve. The results were generally consistent across the three measures. Allelic variation of the Tas1r3 gene influenced taste responsiveness to nonnutritive sweeteners (saccharin, acesulfame-K, sucralose, SC-45647), sugars (sucrose, maltose, glucose, fructose), sugar alcohols (erythritol, sorbitol), and some amino acids (d-tryptophan, d-phenylalanine, l-proline). Tas1r3 genotype did not affect taste responses to several sweet-tasting amino acids (l-glutamine, l-threonine, l-alanine, glycine), glucose polymers (Polycose, maltooligosaccharide), and nonsweet NaCl, HCl, quinine, monosodium glutamate, and inosine 5′-monophosphate. Thus Tas1r3 polymorphisms affect taste responses to many nutritive and nonnutritive sweeteners (all of which must interact with a taste receptor involving T1R3), but not to all carbohydrates and amino acids. In addition, we found that the genetic architecture of sweet taste responsiveness changes depending on the measure of taste response and the intensity of the sweet taste stimulus. Variation in the T1R3 receptor influenced peripheral taste responsiveness over a wide range of sweetener concentrations, but behavioral responses to higher concentrations of some sweeteners increasingly depended on mechanisms that could override input from the peripheral taste system.

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Orgad, S., H. Nelson, D. Segal, and N. Nelson. "Metal ions suppress the abnormal taste behavior of the Drosophila mutant malvolio." Journal of Experimental Biology 201, no. 1 (January 1, 1998): 115–20. http://dx.doi.org/10.1242/jeb.201.1.115.

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A mutation in the malvolio (mvl) gene affects taste behavior in Drosophila melanogaster. The malvolio gene encodes a protein (MVL) that exhibits homology to the mammalian natural resistance-associated macrophage proteins. It is also homologous to the Smf1 protein from Saccharomyces cerevisiae, which we have recently demonstrated to function as a Mn2+/Zn2+ transporter. We proposed that the Drosophila and mammalian proteins, like the yeast SMF1 gene product, are metal-ion transporters. To test this hypothesis, malvolio mutant flies were allowed to develop, from egg to adulthood, on a medium containing elevated concentrations of metal ions. Mutant flies that were reared in the presence of 10 mmol l-1 MnCl2 or FeCl2 developed into adults with recovered taste behavior. CaCl2 or MgCl2 had no effect on the mutant's taste perception. ZnCl2 inhibited the effect of MnCl2 when both ions were supplied together. Similar suppression of the abnormal taste behavior was observed when mvl mutants were fed MnCl2 or FeCl2 only at the adult stage. Furthermore, exposure of adult mutant flies to these ions in the testing plate for only 2 h was sufficient to restore normal taste behavior. The suppression of the defective taste behavior suggests that MVL functions as a Mn2+/Fe2+ transporter and that Mn2+ and/or Fe2+ are involved in the signal transduction of taste perception in Drosophila adults.

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Aroke, Edwin, Keesha Powell-Roach, Rosario Jaime-Lara, Markos Tesfaye, Abhrarup Roy, Pamela Jackson, and Paule Joseph. "Taste the Pain: The Role of TRP Channels in Pain and Taste Perception." International Journal of Molecular Sciences 21, no. 16 (August 18, 2020): 5929. http://dx.doi.org/10.3390/ijms21165929.

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Transient receptor potential (TRP) channels are a superfamily of cation transmembrane proteins that are expressed in many tissues and respond to many sensory stimuli. TRP channels play a role in sensory signaling for taste, thermosensation, mechanosensation, and nociception. Activation of TRP channels (e.g., TRPM5) in taste receptors by food/chemicals (e.g., capsaicin) is essential in the acquisition of nutrients, which fuel metabolism, growth, and development. Pain signals from these nociceptors are essential for harm avoidance. Dysfunctional TRP channels have been associated with neuropathic pain, inflammation, and reduced ability to detect taste stimuli. Humans have long recognized the relationship between taste and pain. However, the mechanisms and relationship among these taste–pain sensorial experiences are not fully understood. This article provides a narrative review of literature examining the role of TRP channels on taste and pain perception. Genomic variability in the TRPV1 gene has been associated with alterations in various pain conditions. Moreover, polymorphisms of the TRPV1 gene have been associated with alterations in salty taste sensitivity and salt preference. Studies of genetic variations in TRP genes or modulation of TRP pathways may increase our understanding of the shared biological mediators of pain and taste, leading to therapeutic interventions to treat many diseases.

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Seta, Yuji, Chihiro Seta, and Linda A. Barlow. "Notch-associated gene expression in embryonic and adult taste papillae and taste buds suggests a role in taste cell lineage decisions." Journal of Comparative Neurology 464, no. 1 (July 10, 2003): 49–61. http://dx.doi.org/10.1002/cne.10787.

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Qin, Yumei, Salin Raj Palayyan, Xin Zheng, Shiyi Tian, Robert F. Margolskee, and Sunil K. Sukumaran. "Type II taste cells participate in mucosal immune surveillance." PLOS Biology 21, no. 1 (January 12, 2023): e3001647. http://dx.doi.org/10.1371/journal.pbio.3001647.

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The oral microbiome is second only to its intestinal counterpart in diversity and abundance, but its effects on taste cells remains largely unexplored. Using single-cell RNASeq, we found that mouse taste cells, in particular, sweet and umami receptor cells that express taste 1 receptor member 3 (Tas1r3), have a gene expression signature reminiscent of Microfold (M) cells, a central player in immune surveillance in the mucosa-associated lymphoid tissue (MALT) such as those in the Peyer’s patch and tonsils. Administration of tumor necrosis factor ligand superfamily member 11 (TNFSF11; also known as RANKL), a growth factor required for differentiation of M cells, dramatically increased M cell proliferation and marker gene expression in the taste papillae and in cultured taste organoids from wild-type (WT) mice. Taste papillae and organoids from knockout mice lacking Spib (SpibKO), a RANKL-regulated transcription factor required for M cell development and regeneration on the other hand, failed to respond to RANKL. Taste papillae from SpibKO mice also showed reduced expression of NF-κB signaling pathway components and proinflammatory cytokines and attracted fewer immune cells. However, lipopolysaccharide-induced expression of cytokines was strongly up-regulated in SpibKO mice compared to their WT counterparts. Like M cells, taste cells from WT but not SpibKO mice readily took up fluorescently labeled microbeads, a proxy for microbial transcytosis. The proportion of taste cell subtypes are unaltered in SpibKO mice; however, they displayed increased attraction to sweet and umami taste stimuli. We propose that taste cells are involved in immune surveillance and may tune their taste responses to microbial signaling and infection.

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Chen, Jingguo, Eric D. Larson, Catherine B. Anderson, Pratima Agarwal, Daniel N. Frank, Sue C. Kinnamon, and Vijay R. Ramakrishnan. "Expression of Bitter Taste Receptors and Solitary Chemosensory Cell Markers in the Human Sinonasal Cavity." Chemical Senses 44, no. 7 (June 20, 2019): 483–95. http://dx.doi.org/10.1093/chemse/bjz042.

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Abstract Some bitter taste receptors (TAS2R gene products) are expressed in the human sinonasal cavity and may function to detect airborne irritants. The expression of all 25 human bitter taste receptors and their location within the upper airway is not yet clear. The aim of this study is to characterize the presence and distribution of TAS2R transcripts and solitary chemosensory cells (SCCs) in different locations of the human sinonasal cavity. Biopsies were obtained from human subjects at up to 4 different sinonasal anatomic sites. PCR, microarray, and qRT-PCR were used to examine gene transcript expression. The 25 human bitter taste receptors as well as the sweet/umami receptor subunit, TAS1R3, and canonical taste signaling effectors are expressed in sinonasal tissue. All 25 human bitter taste receptors are expressed in the human upper airway, and expression of these gene products was higher in the ethmoid sinus than nasal cavity locations. Fluorescent in situ hybridization demonstrates that epithelial TRPM5 and TAS2R38 are expressed in a rare cell population compared with multiciliated cells, and at times, consistent with SCC morphology. Secondary analysis of published human sinus single-cell RNAseq data did not uncover TAS2R or canonical taste transduction transcripts in multiciliated cells. These findings indicate that the sinus has higher expression of SCC markers than the nasal cavity in chronic rhinosinusitis patients, comprising a rare cell type. Biopsies obtained from the ethmoid sinus may serve as the best location for study of human upper airway taste receptors and SCCs.

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Panguluri, Siva K., Nobuyuki Kuwabara, Nigel Cooper, Srinivas M. Tipparaju, Kevin B. Sneed, and Robert F. Lundy. "Gene Network Analysis in Amygdala following Taste Aversion Learning in Rats." Neuroscience Journal 2013 (May 23, 2013): 1–13. http://dx.doi.org/10.1155/2013/739764.

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Conditioned taste aversion (CTA) is an adaptive behavior that benefits survival of animals including humans and also serves as a powerful model to study the neural mechanisms of learning. Memory formation is a necessary component of CTA learning and involves neural processing and regulation of gene expression in the amygdala. Many studies have been focused on the identification of intracellular signaling cascades involved in CTA, but not late responsive genes underlying the long-lasting behavioral plasticity. In this study, we explored in silico experiments to identify persistent changes in gene expression associated with CTA in rats. We used oligonucleotide microarrays to identify 248 genes in the amygdala regulated by CTA. Pathway Studio and IPA software analyses showed that the differentially expressed genes in the amygdala fall in diverse functional categories such as behavior, psychological disorders, nervous system development and function, and cell-to-cell signaling. Conditioned taste aversion is a complex behavioral trait which involves association of visceral and taste inputs, consolidation of taste and visceral information, memory formation, retrieval of stored information, and extinction phase. In silico analysis of differentially expressed genes is therefore necessary to manipulate specific phase/stage of CTA to understand the molecular insight.

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Le Gléau, Léa, Christine Rouault, Céline Osinski, Edi Prifti, Hédi Antoine Soula, Jean Debédat, Pauline Busieau, et al. "Intestinal alteration of α-gustducin and sweet taste signaling pathway in metabolic diseases is partly rescued after weight loss and diabetes remission." American Journal of Physiology-Endocrinology and Metabolism 321, no. 3 (September 1, 2021): E417—E432. http://dx.doi.org/10.1152/ajpendo.00071.2021.

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Our data highlighted 1) the sweet taste transduction pathway in EECs plays pivotal role for glucose homeostasis at least at gene expression level; 2) metabolic disorders led to altered gene expression of sweet taste signaling pathway in intestine contributing to impaired GLP-1 secretion; and 3) after surgical intestinal modifications, increased expression of α-gustducin contributed to metabolic improvement.

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Bachmanov, Alexander A., Danielle R. Reed, Xia Li, and Gary K. Beauchamp. "Genetics of sweet taste preferences." Pure and Applied Chemistry 74, no. 7 (January 1, 2002): 1135–40. http://dx.doi.org/10.1351/pac200274071135.

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Inbred mouse strains display marked differences in avidity for sweet solutions due in part to genetic differences among strains. Using several techniques, we have located a number of regions throughout the genome that influence sweetener acceptance. One prominent locus regulating differences in sweetener preferences among mouse strains is the saccharin preference (Sac) locus on distal chromosome 4. Afferent responses of gustatory nerves to sweeteners also vary as a function of allelic differences in the Sac locus, suggesting that this gene may encode a sweet taste receptor. Using a positional cloning approach, we identified a gene (Tas1r3) encoding the third member of the T1R family of putative taste receptors, T1R3. Introgression by serial back-crossing of a chromosomal fragment containing the Tas1r3 allele from the high sweetener-preferring strain onto the genetic background of the low sweetener-preferring strain rescued its low sweetener-preference phenotype. Tas1r3 has two common haplotypes, one found in mouse strains with elevated sweetener preference and the other in strains relatively indifferent to sweeteners. This study, in conjunction with complimentary recent studies from other laboratories, provides compelling evidence that Tas1r3 is equivalent to the Sac locus and that the T1R3 receptor (when co-expressed with taste receptor T1R2) responds to sweeteners. However, other sweetness receptors may remain to be identified.

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Kokrashvili, Zaza, Karen K. Yee, Erwin Ilegems, Ken Iwatsuki, Yan Li, Bedrich Mosinger, and Robert F. Margolskee. "Endocrine taste cells." British Journal of Nutrition 111, S1 (January 2, 2014): S23—S29. http://dx.doi.org/10.1017/s0007114513002262.

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In taste cells, taste receptors, their coupled G proteins and downstream signalling elements mediate the detection and transduction of sweet, bitter and umami compounds. In some intestinal endocrine cells, taste receptors and gustducin contribute to the release of glucagon-like peptide 1 (GLP-1) and other gut hormones in response to glucose and non-energetic sweeteners. Conversely, taste cells have been found to express multiple hormones typically found in intestinal endocrine cells, e.g. GLP-1, glucagon, somatostatin and ghrelin. In the present study, by immunohistochemistry, multiple subsets of taste cells were found to express GLP-1. The release of GLP-1 from ‘endocrine taste cells’ into the bloodstream was examined. In wild-type mice, even after oesophagectomy and vagotomy, oral stimulation with glucose induced an elevation of GLP-1 levels in the bloodstream within 10 min. Stimulation of taste cell explants from wild-type mice with glucose led to the release of GLP-1 into the medium. Knocking out of the Tas1r3 gene did not eliminate glucose-stimulated GLP-1 release from taste cells in vivo. The present results indicate that a portion of the cephalic-phase rise in circulating GLP-1 levels is mediated by the direct release of GLP-1 from taste cells into the bloodstream.

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Lossow, Kristina, Wolfgang Meyerhof, and Maik Behrens. "Sodium Imbalance in Mice Results Primarily in Compensatory Gene Regulatory Responses in Kidney and Colon, but Not in Taste Tissue." Nutrients 12, no. 4 (April 3, 2020): 995. http://dx.doi.org/10.3390/nu12040995.

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Renal excretion and sodium appetite provide the basis for sodium homeostasis. In both the kidney and tongue, the epithelial sodium channel (ENaC) is involved in sodium uptake and sensing. The diuretic drug amiloride is known to block ENaC, producing a mild natriuresis. However, amiloride is further reported to induce salt appetite in rodents after prolonged exposure as well as bitter taste impressions in humans. To examine how dietary sodium content and amiloride impact on sodium appetite, mice were subjected to dietary salt and amiloride intervention and subsequently analyzed for ENaC expression and taste reactivity. We observed substantial changes of ENaC expression in the colon and kidney confirming the role of these tissues for sodium homeostasis, whereas effects on lingual ENaC expression and taste preferences were negligible. In comparison, prolonged exposure to amiloride-containing drinking water affected β- and αENaC expression in fungiform and posterior taste papillae, respectively, next to changes in salt taste. However, amiloride did not only change salt taste sensation but also perception of sucrose, glutamate, and citric acid, which might be explained by the fact that amiloride itself activates bitter taste receptors in mice. Accordingly, exposure to amiloride generally affects taste impression and should be evaluated with care.

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Dolgov, S. V., V. G. Lebedev, and F. P. Firsov. "PEAR FRUIT TASTE MODIFICATION BY THAUMATIN II GENE EXPRESSION." Acta Horticulturae, no. 909 (October 2011): 67–73. http://dx.doi.org/10.17660/actahortic.2011.909.5.

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Wong, Gwendolyn T., Luis Ruiz-Avila, and Robert F. Margolskee. "Directing Gene Expression to Gustducin-Positive Taste Receptor Cells." Journal of Neuroscience 19, no. 14 (July 15, 1999): 5802–9. http://dx.doi.org/10.1523/jneurosci.19-14-05802.1999.

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Ikeda, Minoru. "The Study of the Taste Receptor Gene for Dysgeusia." Otolaryngology–Head and Neck Surgery 143, no. 2_suppl (August 2010): P175. http://dx.doi.org/10.1016/j.otohns.2010.06.849.

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Fukabori, R. "POMC gene expression is induced by the taste stimulation." Neuroscience Research 38 (2000): S114. http://dx.doi.org/10.1016/s0168-0102(00)81531-x.

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Panguluri, Siva K., Nobuyuki Kuwabara, Yi Kang, Nigel Cooper, and Robert F. Lundy. "Conditioned taste aversion dependent regulation of amygdala gene expression." Physiology & Behavior 105, no. 4 (February 2012): 996–1006. http://dx.doi.org/10.1016/j.physbeh.2011.11.001.

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Nishimura, Azusa, Yuko Ishida, Aya Takahashi, Haruka Okamoto, Marina Sakabe, Masanobu Itoh, Toshiyuki Takano-Shimizu, and Mamiko Ozaki. "Starvation-Induced Elevation of Taste Responsiveness and Expression of a Sugar Taste Receptor Gene inDrosophila melanogaster." Journal of Neurogenetics 26, no. 2 (June 2012): 206–15. http://dx.doi.org/10.3109/01677063.2012.694931.

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Wooding, Stephen P., Vicente A. Ramirez, and Maik Behrens. "Bitter taste receptors." Evolution, Medicine, and Public Health 9, no. 1 (January 1, 2021): 431–47. http://dx.doi.org/10.1093/emph/eoab031.

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Abstract Bitter taste perception plays vital roles in animal behavior and fitness. By signaling the presence of toxins in foods, particularly noxious defense compounds found in plants, it enables animals to avoid exposure. In vertebrates, bitter perception is initiated by TAS2Rs, a family of G protein-coupled receptors expressed on the surface of taste buds. There, oriented toward the interior of the mouth, they monitor the contents of foods, drinks and other substances as they are ingested. When bitter compounds are encountered, TAS2Rs respond by triggering neural pathways leading to sensation. The importance of this role placed TAS2Rs under selective pressures in the course of their evolution, leaving signatures in patterns of gene gain and loss, sequence polymorphism, and population structure consistent with vertebrates' diverse feeding ecologies. The protective value of bitter taste is reduced in modern humans because contemporary food supplies are safe and abundant. However, this is not always the case. Some crops, particularly in the developing world, retain surprisingly high toxicity and bitterness remains an important measure of safety. Bitter perception also shapes health through its influence on preference driven behaviors such as diet choice, alcohol intake and tobacco use. Further, allelic variation in TAS2Rs is extensive, leading to individual differences in taste sensitivity that drive these behaviors, shaping susceptibility to disease. Thus, bitter taste perception occupies a critical intersection between ancient evolutionary processes and modern human health.

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Zhong, Huaming, Shuai Shang, Xiaoyang Wu, Jun Chen, Wanchao Zhu, Jiakuo Yan, Haotian Li, and Honghai Zhang. "Genomic evidence of bitter taste in snakes and phylogenetic analysis of bitter taste receptor genes in reptiles." PeerJ 5 (August 18, 2017): e3708. http://dx.doi.org/10.7717/peerj.3708.

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As nontraditional model organisms with extreme physiological and morphological phenotypes, snakes are believed to possess an inferior taste system. However, the bitter taste sensation is essential to distinguish the nutritious and poisonous food resources and the genomic evidence of bitter taste in snakes is largely scarce. To explore the genetic basis of the bitter taste of snakes and characterize the evolution of bitter taste receptor genes (Tas2rs) in reptiles, we identifiedTas2rgenes in 19 genomes (species) corresponding to three orders of non-avian reptiles. Our results indicated contractions ofTas2rgene repertoires in snakes, however dramatic gene expansions have occurred in lizards. Phylogenetic analysis of theTas2rs with NJ and BI methods revealed thatTas2rgenes of snake species formed two clades, whereas in lizards theTas2rgenes clustered into two monophyletic clades and four large clades. Evolutionary changes (birth and death) of intactTas2rgenes in reptiles were determined by reconciliation analysis. Additionally, the taste signaling pathway calcium homeostasis modulator 1 (Calhm1) gene of snakes was putatively functional, suggesting that snakes still possess bitter taste sensation. Furthermore, Phylogenetically Independent Contrasts (PIC) analyses reviewed a significant correlation between the number ofTas2rgenes and the amount of potential toxins in reptilian diets, suggesting that insectivores such as some lizards may require moreTas2rs genes than omnivorous and carnivorous reptiles.

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Nor, N. B. M., M. A. Fox, I. R. Metcalfe, and W. J. Russell. "The Taste of Intravenous Thiopentone." Anaesthesia and Intensive Care 24, no. 4 (August 1996): 483–85. http://dx.doi.org/10.1177/0310057x9602400412.

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Patients sometimes notice an onion or garlic taste before losing consciousness with thiopentone. An assessment of 113 patients revealed that 42% of patients noticed this taste. The effect was observed less in older patients. There was no statistically significant difference in the incidence between men and women. Premedicated patients had a lower incidence, but this was explained by the greater proportion of older patients receiving a premedication. If the taste effect of thiopentone is genetically determined then it is a different gene to thiocarbamate which has about 75% tasters.

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Worku, Mulumebet, and Kingsley Ekwemalor. "PSVI-7 Variation in bitter taste receptor genes in three breeds of goats." Journal of Animal Science 97, Supplement_3 (December 2019): 206. http://dx.doi.org/10.1093/jas/skz258.424.

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Abstract The objective of this study was to detect bitter taste receptor (T2Rs) variants in three breeds of goats. The ability to taste bitter taste impacts feed intake, digestion, and rejection of potentially toxic substances. Blood was collected from three breeds of goats (Spanish, Savannah, and Boer n = 5 /breed). Genomic DNA was extracted. The concentration and purity of DNA was determined using the Nanodrop spectrophotometer. Primers specific for seven T2R gene variants (T2R3, T2R4, T2R10, T2R12, T2R13, T2R16, and T2R67) were used to detect the goat T2R gene based on average threshold cycle. DNA products were commercially sequenced (Eurofins Genomics). The sequenced products were used in BLAST against the Capra hircus redundant nucleotide database. All seven taste gene variants were detected in the Savannah breed, In Spanish goats T2R4 and T213 were not detected, In Boer goats only T2R3, T2R16 and T2R13 were detected. Polymorphisms in T2R impact dietary preference, innate immunity and health. Thus, studies are needed to ascertain the possible functional significance of this variation using a larger sample size

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Indriani, Fenny, Rike Oktarianti, and Syubbanul Wathon. "Genetic Study of Phenylthiocarbamide (PTC) Taste Sensitivity In Population of The Osing in Kemiren Village-Banyuwangi." BERKALA SAINSTEK 9, no. 1 (April 30, 2021): 1. http://dx.doi.org/10.19184/bst.v9i1.19844.

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The ability to taste phenylthiocarbamide (PTC), is autosomal trait inherited in a simple Mendelian recessive pattern. The frequency of Taster and non-Taster allele is varies in different populations. The purpose of the research is to investigate the prevalence, gene frequency and genotype frequency of taster (T) and non taster (ts of Osing population in Kemiren-Banyuwangi. PTC serial dilution method was used to assess the PTC Taster and non-Taster phenotypes. The Hardy–Weinberg method was used to determine allele frequencies. The total of samples were 227 people, male were 117 and female were 110 with age range of 15–30 years were randomly selected. The result showed that the Osing population as Taster were 210 (92,52%) and non Taster were 17samples (7,48%) . The allele frecuency of Taster (T) was 0,73 and non Taster (t) was 0,27 respectively. The genotype frequency of dominant Taster (TT) was 0,54, heterozygosity Taster (Tt) was 0,39, and genotype of non Taster (tt) was 0,07.

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Journal articles on the topic 'Taste gene'

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