BMA ASSIGNMENT
1
Abstract
This study delves into the genetic basis of phenylthiocarbamide (PTC) tasting, aiming
to understand why some individuals perceive PTC as intensely bitter (tasters) while
others cannot detect its bitterness (non-tasters). Taste perception is mediated by
specialized receptors, with bitter taste being primarily attributed to TAS2R38 gene
variations. This study focuses on the C785T mutation within the TAS2R38 gene and
its influence on phenylthiocarbamide (PTC) taste perception. The objective was to
determine if there was a significant difference in the allele frequencies (taster and
non-taster) of the C785T SNP between Batch 9 students(Sri Lanka) and South Asians
and African Americans. The methodology involved DNA extraction, PCR
amplification, Fnu4HI restriction enzyme digestion, and agarose gel electrophoresis.
This allowed for the assessment of TAS2R38 genotypes among 18 individual in batch
9. Gel image from the electrophoresis process was obtained of the batch 9 individuals.
These results were acquired inorder to assess the genotype frequencies and allele
frequencies for PTC taste perception in individuals of batch 9. Blast tool was used to
obtain the DNA sequence of the gene and NCBI tool was used to obtain data on the
gene. Genotype frequencies and allele frequencies of the batch 9 individuals was
calculated aided by the gel image.genotype frequencies revealed that 67% was tasters
whereas 33% of individuals were non-tasters. Moreover allele frequencies showed
55% unmutated whereas 44% mutated allele. These data confirms that batch 9 has
more
tasters for PTC compared to non-tasters.Batch 9 Allele frequencies were
compared with south asians and african amermeicans. Chi-square test was carried out
using minitab to obtain the correlation between batch 9 individuals compared to south
Asians and African American populations. The P-value obtained was 0.000 which
denotes to the fact that there is a significant difference between the alleles of batch 9
individuals(sri lanka) compared to south asians and african americans.
2
Introduction
The intension of the study is to find why some people taste and why some people do
not taste PTC(bitter).
Taste perception is mediated by specialized taste receptors located on the oral cavity
(Behrens & Meyerhof, 2006). It is assumed that the sense of taste can distinguish five
primary sensory qualities (sweet, sour, salty, bitter and umami).When water-soluble
molecules in the mouth come into touch with the taste buds' epithelial cells, taste
perception occurs. separate processes, mediate the perception of the diverse flavors.
G-protein-coupled heterodimer receptors (GPCRs) mediate the transmission of umami
and sweetness:taste receptor type 1 member 2 (T1R2) + T1R3 sweet and T1R1 +
T1R3 umami. The GPCR T2R family reacts to a variety of bitter taste compounds.
(Melis, M., & Tomassini Barbarossa, I. 2017). One of the well-studied taste qualities
is bitterness, which serves as a protective mechanism against the ingestion of
potentially harmful substances. The perception of bitterness is primarily attributed to
the activation of bitter taste receptors known as TAS2Rs (Taste 2 Receptors)
(Meyerhof, et al., 2010).
Fig 01- Taste receptors of sweet, sour, salty, bitter and umami (Martin, L.T.P., Dupré,
D.J.,2016)
3
TAS2Rs are G-protein-coupled receptors (GPCRs) that are expressed in taste receptor
cells. These receptors play a pivotal role in detecting a wide range of bitter
compounds found in various foods and drinks. Among these TAS2Rs, TAS2R38 is
one of the most well-known, and it is responsible for the perception of the bitter
compound phenylthiocarbamide (PTC) and its chemical analog 6-n-propylthiouracil
(PROP). PTC taste perception is genetically determined, with some individuals being
"tasters" who perceive PTC as intensely bitter and others being "non-tasters" who
cannot detect its bitterness (Wooding., 2006).
Bitter taste perception, particularly the ability to detect phenylthiocarbamide (PTC), is
strongly influenced by genetic variations in the TAS2R38 gene. TAS2R38 encodes a
G protein-coupled receptor responsible for recognizing bitter compounds (Kim, et al.,
2003).TAS2R38 has several single nucleotide polymorphisms (SNPs), with the most
notable ones being PAV (proline-alanine-valine) and AVI (alanine-valine-isoleucine)
haplotypes. (Hayes, et al., 2011).
hree key single nucleotide polymorphisms (SNPs) within this gene significantly
impact one's sensitivity to PTC (Kim, et al., 2003):
145C→G (P49A): cytosine (C) with guanine (G) at position 145, directing to
an amino acid change from proline (P) to alanine (A) at position 49 (P49A) in
the TAS2R38 protein.
785C→T (A262V): At position 785, the cytosine (C) is replaced by thymine
(T), resulting in an amino acid substitution from alanine (A) to valine (V) at
position 262 (A262V) in the TAS2R38 protein.
886G→A (V296I): The guanine (G) at position 886 is mutated to adenine (A),
leading to a valine-to-isoleucine substitution at position 296 (V296I) in
TAS2R38.
All theses SNPs further impairs the receptor's ability to interact with PTC,
contributing to reduced sensitivity in individuals..
4
Table
1-several
single
nucleotide
polymorphisms
of
TAS2R38
(SNPs)(https://www.minipcr.com/wpcontent/uploads/KT100403_miniPCR_PTC_ta
ster_student_guide_V2.1_041322.pdf)
The combination of these three SNPs defines the TAS2R38 haplotypes. Individuals
with two copies of the PAV haplotype (P49A, A262V, V296I) are generally strong
tasters of PTC, while those with two copies of the AVI haplotype (lacking these
mutations) are non-tasters. Heterozygotes, carrying one copy of each haplotype,
exhibit intermediate PTC sensitivity (Kim, et al., 2003). The practical investigates the
SNP polymorphism at position 785C-T.
In the case of the TAS2R38 gene, the original sequence in the Taster allele contains
the Fnu4H1 is an endonuclease enzyme that identifies specific DNA sequences,
referred to as restriction sites, and splits the DNA at these sites(Orrù, R et al.,
2015).The elimination of the Fnu4H1 restriction site in the TAS2R38 gene is a
consequence of a specific genetic mutation that replaces cytosine (C) with thymine (T)
at position 785 (C785T) in the Non-Taster allele (Risso, et al., 2016). This mutation
disrupts the recognition sequence for the Fnu4H1 restriction enzyme
5
Fig 2- Restriction enzyme cutting site (http://www.hcrowder.com/pcr.html)
This mutation-induced loss of the Fnu4H1 restriction site serves as a genetic marker
for distinguishing between Taster and Non-Taster alleles in the TAS2R38 gene and
has been widely used in genetic studies to identify and classify individuals based on
their bitter taste perception genotype (Risso, et al., 2016)
As evaluated in the objective, the hypothesis that is elaborated in this study
programme is as follows:
Ho- – There is no significant difference between the allele frequencies (taster and
non-taster) between the batch 9 allele frequency and south Asians and African
Americans.
Ha– There is a significant difference between the allele frequencies (taster and
non-taster) between the batch 9 allele frequency and south Asians and African
Americans.
So therefore,if the
P<0.05- Reject null hypothesis/accept alternative hypothesis (Ha)
P> 0.05 – Do not reject null Hypothesis (H0)
6
Methods
Materials
Table 2: Materials
Reagents
1. DNA Extraction
Consumables

Buccal cells

Labeled tubes

Proteinase K

sterile wooden

Chelex suspension

sterile plastic loop

Centrifuge machine

Eppendorf
tubes
(1.5 ml)

Nanodrop
mechanism
DNA
for
purity
measurement
2.
PCR
(Polymerase

PCR primer mix

PCR tubes

DNA template

Thermal cycler
Fnu4HI restriction

PCR tubes (stored)
enzyme

0.5 ml Eppendorf
Chain Reaction)
3.
Restriction
Enzyme

Digestion:
master
mixture
tubes

Heating block at
37°C

4.
Agarose
Electrophoresis:
Gel

Agarose gel (2%)

TBE buffer

Ethidium Bromide

Geneflow tanks or
Peqlab/Hybaid
7
(for gel staining)

tanks

DNA ladder (100
bp)

UV
transilluminator for
gel visualization

Methodology
1. DNA extraction
Firstly, inorder obtain the sample cells, a sterile wooden was used to scrap the inside
of the cheeks to remove loose buccal cells.
The cheek cells in the wooden splint was scraped off using a sterile plastic loop. The
loop was twirled in a 1.5ml eppendorf tube containing 350µl 5% Chelex suspension
Precipitation of DNA is done as follows;
i. 4 μl of Proteinase K was added to 1.5 ml eppendorf containing cheek cells
& Chelex.
ii. Sample was incubated 30 minutes under 56 °C
iii. Tube was vortexed for 10 seconds.
iv. Tube was placed in the centrifuge machine and balanced it. Tube is centrifuged at
13000 rpm for 20 seconds.
v. Tube was then placed for 15 min under 98 Celsius.
vi. Tube was then vortexed for 10 seconds and centrifuged for 3 minutes in the
maximum speed.
Vii. The
supernatant (liquid above the chelex), containing buccal cell DNA
(Template ), was transfered to a new 1.5 ml Eppendorf tube.
Viii. An aliquot (5 µl) of the sample was placed in an eppendorf tube labelled with
initials. This aliquot/tube was measured using the nanodrop nucleic acid measurement
machine
2. PCR
8
i.
43 µl of master mix and 6.5 µl of DNA template(buccal cell DNA) were added to
the tube.
ii. Solution was mixed by flicking with a finger to dissolve and pulse spinned to
gather the liquid content at the bottom.
iii. Tube was located in the rack (with the lid tightened) for thermal cycling.
iv. The PCR was initiated using 5 distint temperatures, at first heat gor 94˚C for 4
minutes.Secondly, at 55˚C, 72˚C , 94˚C
for 40 seconds. These 3 temperatures for
repeated for 40 cycles. Thirdly, at 55˚C
for 5 minutes and finally for 72°C for 5
minutes.
3. Restriction enzyme(Fnu4HI) digestion
i.
aliquot (20 µl) from the PCR tube was added to a 0.5ml eppendorf tube already
containing 10 µl of Fnu4HI restriction enzyme master mixture, which contained
30 µl.
ii. Tube was mixed by fliking with fingers and centrifuged a while. Then it is kept in
37°C heating water bath.
iii. Tube was left for 2hr, inorder for the Fnu4HI restriction enzyme digest.
4. Agarose gel electrophoresis
i.
Tube with undigested(remaining PCR reaction volume) DNA were taken
carefully.
ii. The Fnu4HI restriction enzyme digest was obtained
iii. 2% submerged agarose gel were set;with 70 ml, Peqlab Geneflow tanks
(PurpleLids, 12 well comb) / or with 50ml agarose, Hybaid tanks (10 well comb)
were left to set
iv. PCR tube containing 3 µl of DNA loading buffer was added to a tube containing
12 µl PCR/R Enzyme digest.
And simultaneosly, 3 µl of DNA loading buffer (x5) was added to a tube containing
12 µl residual PCR.
v.
Both tubes (total 15 µl) were Mixed (finger) and pulse spinned and add 8 – 10 µl
of this mixture to a 2% agarose gel submerged in TBE buffer noting the lanes you
have loaded (UD & Digested).
vi. 8-10 µl of 100 bp DNA Ladder was added to the remaining well as a DNA
marker
9
vii. Electrophoresis was performed at 90 V for 45min until blue marker is halfway
through gel
viii. A Photograph was taken of the gel under UV transillumination.
10
RESULTS
GEL IMAGE
Fig 3- Class gel image
My lane is noted as well 13, with 1 band , showing an homozygous mutant with a non
taster for bitter.
11
BLAST - Result
Fig 4- Full report of rs1726866
Fig 5-exon count(1) and position of gene (Location 7p34)
12
Fig 6 - Accession code(NC_000007.14) for the DNA sequence
Fig 7-DNA sequence of the gene
The putative taster receptor TAS2R38 gene full FASTA sequence for Homo sapiens
is obtained after blasting the forward and backward primer sequence. The betaglucopyranoside-induced bitter taste is mediated by the TAS2R38 gene, a potential
taster receptor for homo sapiens. This DNA sequence's accession number is
NC_000007.14.
13
Fig 8- coding region highlighted of the mRNA sequence.
Fig 9-stop codon start codon of mRNA, gene and CDS(coding sequence)
14
Fig 10-Complete report on the potential taster receptor gene TAS2R38 in humans on
the coding pattern
15
Fig11- The whole conding sequence of the human candidate taste receptor gene
TAS2R38 FASTA sequences
mRNA sequence starting and ending positions
Coding sequence starting and ending positions
Fig 12-difference in the starting and ending sequence positions between the mRNA
and coding sequence.
16
3 SNP mutations
=CCA-GCA at 145pb
=GCT- GTT at 785bp
=GTC- ATC at 866bp
Fig 13-SNP’s (single nucleotide polymorphisms) positions indicated in the gene,
reported between tasters & non-tasters located on the coding sequence.
Fig 14- indications of forward primer, backward primer, start codon and
termination codon
17
Fig 15-Entire Report of coding sequence
18
GCA-AVI
GTT-VAI
AVI- Non taster
ATC-ILE
Fig 16-SNP mutations on the coding sequence simultaneously indicated the mutations
result in the protein sequence
Figure 17: mRNA sequence of the Homo sapiens’ candidate taster receptor TAS2R38
gene (Accesssion code -NM_176817.5)
19
Fig 18-Protein sequence for the taste receptor type 2 member 38
Fig 19-: protein alignments for the potential taste receptor in humans, TAS2R38
20
Fig 20- Displays the data about the Protein,333 amino acids and
Fig 21- The TAS2R38 gene is found on chromosome 7 in humans.
21
Figure 22- shows the SNP variables for rs1726866.Reference SNP report
22
CALCULATIONS
(CC)
AA
(100% taster)
(Homozygous
Wild)
(CT)
Aa
(50% taster)
(Heterozygous)
(TT)
aa
(0% taster/non taster)
(Homozygous mutant)
Fig 23-Expansion of genotypes
Table 3-Class Gel picture broad analysis of genotypes
Lane
Genotype
A
a
Genotype(Type)
2
aa
0
2
Homozygous
mutant
3
AA
2
0
Homozygous
wild
4
AA
2
0
Homozygous
wild
5
Aa
1
1
Heterozygous
6
aa
0
2
Homozygous
mutant
7
AA
2
0
Homozygous
wild
8
Aa
1
1
Heterozygous
9
Aa
1
1
Heterozygous
10
aa
0
2
Homozygous
mutant
11
AA
2
0
Homozygous
wild
13-My
aa
0
2
intended lane
14
Homozygous
mutant
AA
2
0
Homozygous
wild
23
15
Aa
1
1
Heterozygous
16
Aa
1
1
Heterozygous
17
aa
0
2
Homozygous
mutant
18
AA
2
0
Homozygous
wild
19
AA
2
0
Homozygous
wild
20
Aa
1
1
Heterozygous
Table 4- Genotype & Phenotype
Genotype
Genotype alleles
Homozygous wild AA
Phenotype
Taster
type
Heterozyogous
Aa
Taster
Homozygous
aa
Non-taster
mutant
GENOTYPE FREQUENCY
AA genotype frequency = No. of AA individuals
{n(AA)+n(Aa)+n(aa)}
 AA genotype frequency= 7
18
=0.3888 Ω 0.389
 Aa genotype frequency=5
18
=0.2777Ω 0.278
 Aa genotype frequency=6
18
=0.3333 Ω 0.333
24
ALLELE FREQUENCY
Total number of alleles;
 A Alleles:
{(nAA)×2 ＋(nAa)×1}
{(7)×2+(6)×1}
=20
 a Alleles
{(naa)×2 ＋(nAa)×1}
{(5)×2＋(6)×1}
=16
Allele frequency = Total A alleles in the study group
Total alleles (A+a)in the study group
Allele Frequency of A=20
36
=0.5555
=0.5555×100
=55.55%
Allele Frequency of a=16
36
=0.4444
=44.44%
P-VALUE -CHI SQUARE CALCULATION(MINITAB)
Table 5- Reference allele and alternative allele in populations
Population
Reference
Alternative
allele(Ref)
allele(Alt)
25
South Asians
G=0.3736(37%)
A= 0.6264(62%)
African Americans
G=0.67087(67%)
A=0.32913(33%)
Batch 9 class
C=0.5555(56%)
T=0.4444(44%)
As shown in the table NCBI has provide complementary base of the Reference and
alternative allele as G and A instead of C and T. Inorder for precise results the
decimals value are converted into whole numbers, to generate results for the chisquare test.
Fig 24 - Chi squared analysis (minitab) results comparing the allele frequencies of
the Batch 9 group vs African & East Asian groups.
26
Discussion
When it comes to preventing humans from swallowing naturally hazardous
compounds, which often taste bitter, the ability to perceive bitterness plays a crucial
role. Phenylthiocarbamide (PTC) taste sensitivity variation is one of the most wellknown examples.(M. Fareed et al., 2012)
During the methodology, Chelex Suspension was used to inactivate metal ions that
protect the DNA from degradation during. Following that, Proteinase K was added to
break down proteins, including those associated with cellular components, releasing
the DNA into the solution. The master mix contains, DNA polymerase, primers,
nucleotides, and buffer. PCR temperature cycles: Denaturation (94°C): To separate
the DNA strands. Annealing (55°C): to enable primers to bind to the DNA template's
complementary sequences selectively. Extension (72°C): To enable DNA polymerase
to synthesize a new DNA strand based on the template.Next, addition of restriction
enzyme(Fnu4HI) digestion , employed to cut DNA at specific recognition sequences.
Ultimately, Ethidium Bromide was added to stain the DNA that fluoresces under UV
light, allowing to visualize DNA fragments. Loading Buffers, facilitate the loading of
DNA samples into the wells of the gel and to track the progress of electrophoresis.
As displayed in the gel picture, my intended lane is lane number 13. Which displays
an Homozygous mutant, with aa representation, followed by 2 non-taster
alleles(aa).The band on the gel picture lies on the 303bp Which denotes to the fact
that there is a gene mutation which results non-taster phenotype feature, 0% taster
allele. The Fnu4H1 restriction enzyme receptor is not perfectly shaped restricting the
Fnu4H1 restriction enzyme fit with the receptor and cleave the allele, both the alleles
are not cut, both the alleles are mutated, which results in no bitter taste perception. as
shown in fig 3, In lane 13 both the genotypes CC(non-mutated) is replaced with TT
(mutated)
due to the SNP at 785th position.Furthermore,
amino acid sequence
changes from alanine to valine.
Table 3 shows that 18 students examined 18 distinct samples. The overall outcome
reveals dominant and recessive samples. The phenotype of dominant (homozygous
wild type and heterozygous) samples perceives the bitter taste of PTC, but the
phenotype of recessive (homozygous mutant) samples does not taste PTC. Out of 18
27
samples, 13 samples exhibit dominant traits associated with the capacity to taste PTC,
whereas 5 samples exhibit recessive traits associated with the inability to perceive
bitter. Through deliberation of the genotype frequency, 39% of the individuals are
homozygous wild(with CC) type,whereas 33%(CT) are heterozygous and 28% of
individuals are homozygous mutant(TT), table 4. Ultimately 72% of individuals in the
class taste for bitter, whilst 28% do not have the ability to taste bitter perception. The
allele frequencies of batch 9 students simultaneously, elaborated that number of taster
alleles was greater than number of non taster alleles . supporting the fact 55% taster
alleles and 44% non-taste alleles were deliberated.
By considering the study (Amos okutuse., 2018) in Jomo Kenyatta university ,It can
be seen that fewer people were able to taste PTC at the lowest concentration as
opposed to those who were able to taste it at the highest concentration of 0.13.
Additionally, non-tasters at the concentration level of 0.001 PTC was greater than that
at the concentration level of 0.13, providing strong evidence that the number of
people who could taste PTC grew with its rising concentration(Fig 25).Therefore, it
can be inferred from the information provided that the population contains more
tasters as concentration increases.This study supports our class results.
28
Fig 25-PTC tasting data for Jomo Kenyatta university in biostatics class.(Amos
okutuse., 2018)
The PCR product size is 303(highlighted in gel picture), this band has a greater
intensity when compared with the other bands, and this band do not move further due
to increase weight, 300bp was denoted since it lies at a little further from the 300bp
labeled in the ladder.
One coding exon, 1002 base pairs length and encoding a 333 amino acid, 7transmembrane domain G protein-coupled receptor, makes up the TAS2R bitter taste
receptor gene family, the major gene TAS2R38 on chromosome 7 responsible for this
trait has been identified. This receptor responds to bitter stimuli.(Hussain, R.,et 2014).
The marker bands (ladder) in show how many base pairs are present in each band.
When both homozygous dominant alleles (AA) are present, restriction enzymes split
the gene into two pieces, as seen in samples 14, 18, and 19. As seen in samples 15, 16,
and 20, when one allele splits into two and the other stays the same, a gene with a
heterozygous dominant allele (Aa) is broken into three parts by a restriction enzyme.
Both of these genes provide favorable PTC taste results. Individuals who do not
experience the PTC taste in sample 13 and 17 demonstrate that when the gene is not
disrupted by the restriction enzymes, it includes both recessive alleles (tt) represents a
one band due to original size(Fig- 3) (Serackis, et al., 2018).
Table 6- Genotype frequency among different human populations for PTC
tasting.(M.Fareed, et al., 2012)
This populations shows a greater TT and Tt genotype compared to tt.As corellates
with the class population.
Base pair is denoted as 'bp' in the gel electrophoresis picture. Due of their lightness,
shorter bands move upward the membrane. Since the restriction enzymes fail to split
29
the 't' allele due to the presence of the SNP.The original bp will have 303bp whereas
the 2 cutting products will be 238bp and 65bp . ‘t’ band is 303bp, one ‘T’ is 238bp
and other one is 65bp. Due to having a highest number of base pairs ‘t’ does not travel
higher in the gel image due to the weight. ‘T’ travels higher due to having lighter
number of base pairs that are cleaved by the restriction enzymes.
Through comparative inspection of the reference allele(unmutated allele) and
alternative allele(mutated allele) of the 3 populations shown in table 4, reference
allele of Africans Americans are significantly higher, demonstrating 67% compared
to South Asians(37%) and Batch 9(62%).To recapitulate that African Americans have
greater population who with less mutations and more individuals who taste PTC.
However, South Asians have a greater alternative allele of 62% compared to African
Americans(33%) and Batch 9(44%) validating that South Asians population has
increased population with mutations resulting more individuals that do not taste PTC.
Table 7-Allele frequencies among different populations for PTC tasting(M.Fareed, et
al., 2012)
As illustrated, in this population ,both females and males,non taster alleles(t) In
populations in Europe, the prevalence of the non-taster allele T ranges from 25% to
57%. Different castes and ethnic groups in India exhibit diversity in the frequency of
the t-allele. Little variance in the non-taster allele among six populations is revealed
by our investigation.When two racial groups are compared, they differ in phenotype
as they do in genotype for the bitter taste gene, TAS2R38. It is well recognized that a
30
variety of human groups exhibit varying gene frequencies due to a variety of factors,
including mutation, natural selection, inbreeding, genetic drift, and miscegenation.(M.
Fareed et al., 2012)
In the bitter taste gene when considering the mRNA and coding gene, they sequences
start from different positions. In the mRNA strand the sequence starts from 1 where as
the coding sequence starts from 85.Therefore although the mRNA sequence starts
from position 1, coding sequence which codes for the protein sequence starts from 85,
additionally mRNA sequence ends at 1143 and coding sequence ends at 1085,
demonstrating that they have a significant difference in coordinates. Therefore since
the change is occuring in the protein , the SNP should be located in the coding
sequence as shown in fig 13,starting from 85 and ending from 1085.
When digging in research analysis, The prevalence of taste blindness was observed to
be 28% in healthy people and 81% in obese people. Results show a significant
relationship between obesity and non-tasters. When compared to children that are
overweight or obese, it has been observed that non-obese children have a higher
prevalence of the PTC taster characteristic. (Veluswami, D.,
Et.,2015).
There are versatile clinical relevance of tasters and non-tasters of PTC.Due to its link
with food preferences, nutrient intake, and potential health consequences, the
phenylthiocarbamide (PTC) taste ability, which is influenced by the proximity of
certain alleles, has therapeutic significance. Aversions to bitter foods, such as
cruciferous vegetables, may be displayed by people with taster alleles, who are more
sensitive to bitter tastes. This may affect their dietary preferences and result in
inadequate nutrient intake. On the other hand, non-tasters are less sensitive to bitter
flavors and can be more receptive to certain meals.(Tepper, B. J.,et al., 1998). Due to
its potential to customize dietary advice and therapies, this genetic characteristic is
significant in therapeutic practice. To improve dietary adherence and overall health
outcomes, healthcare providers might modify dietary regimens based on a person's
PTC genotype.(Kim, U. K.,et al., 2005). Understanding PTC genotype can also
contribute to research on taste perception and its link to broader health issues, such as
obesity and chronic diseases. It highlights the intricate interplay between genetics and
nutrition,
paving
the
way
for
more
targeted
and
effective
dietary
31
interventions.(Drewnowski, A., et al., 2010). In the field of bitter taste transduction,
PTC presents a remarkable opportunity. Given that it is a gene known to have a
substantial influence on phenotypic in vivo, there are several opportunities for
research of taste physiology, biochemical function, and molecular structure in the
human taste sensitivity.(M.Fareed, et al., 2012)
Finally veiling the objective, that intensity of PTC taste perception is result due to the
presence and absence of C785T SNP. As mentioned earlier, if the P<0.05- Reject null
hypothesis/accept alternative hypothesis (Ha) and if the P> 0.05 – Do not reject null
Hypothesis (H0). As the chi square results been generated in Fig 24, has tabulated that
p=0.000 which is less than 0.05, which supports the statement to Accept the
alternative hypothesis(Ha). Validates the assertion that
there is a significant
difference between the alleles (taster and non-taster) of batch 9 students compared to
South Asians and African Americans. Evaluating that different populations have
various amount of individuals with taster and non-taster for PTC.
CONCLUSION
Ultimately, the p value 0.000 conclude that there is a significant difference of the
batch 9 students (Sri Lanka) compared to South Asians and African Americans.
Accepting the alternative hypothesis.
32
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okutuse
(2018).
Phenylthiocarbamide
(PTC)
Tasting
Lab
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Drewnowski, A., & Almiron-Roig, E. (2010). Human perceptions and preferences for
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Hayes, J. E., Wallace, M. R., Knopik, V. S., Herbstman, D. M., Bartoshuk, L. M., &
Duffy, V. B. (2011). Allelic variation in TAS2R bitter receptor genes associates with
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Table
1-several
single
nucleotide
polymorphisms
of
TAS2R38
(SNPs)(https://www.minipcr.com/wpcontent/uploads/KT100403_miniPCR_PTC_tast
er_student_guide_V2.1_041322.pdf)
http://www.hcrowder.com/pcr.html
35