Diagnosis
of Heterozygous CF Patients afflicted with
c.233dupT
Mutation using Allele Specific PCR
By:
Alisha Ungkuldee, Nicole Curtis, and Sara Kostecka
LB145
Cellular and Molecular Biology
Tuesday
and Thursday 3 PM
Hayden
Stoub and Marla Nazee
11/21/2017
Abstract
The c.233dupT mutation
of the cystic fibrosis transmembrane conductance regulator (CFTR) is a
frameshift mutation found in primarily Hispanic subjects, causing a severe form
of cystic fibrosis (CF) (Gregoire-Bottex and Soe, 2017). The addition of an
extra thymine at the 233rd base pair on exon 3 of the CFTR gene produces a
dysfunctional protein after translation, inhibiting chloride ion movement
through epithelial cells (Gregoire-Bottex and Soe, 2017). Polymerase chain
reactions (PCR) and gel electrophoresis were used to replicate and display the
segment of interest of the CFTR gene in order to determine if DNA tested was
wild-type or had the c.233dupT mutation. We hypothesize that primers designed
with the Yaku-Bonczyk method for a diagnostic assay of the c.233dupT CFTR
mutation will yield an adequate volume of amplified base pair products through
PCR due to increased annealing precision by intentional nucleotide mismatches
at the 3 end. Our team utilized six primers including forward and reverse
mutant primers from Johns Hopkins Lab, MD (Fprimer1 and Rprimer1), designed
forward and reverse primers for the wild-type DNA allele (Fprimer2 and
Rprimer2), and designed forward and reverse primers for the mutant DNA allele
(Fprimer3 and Rprimer3). The annealing temperature for Fprimer1 and Rprimer1
was 52℃ for the first seven cycles and 68℃ for the remaining 23
cycles. An online theoretical annealing temperature calculator by IDT was
utilized to calculate the annealing temperature for the designed primers;
54.7℃ for both Fprimer2 and Rprimer2 and 54.2℃ for both Fprimer3
and Rprimer3 (SantaLucia, 1998). We predict an amplified base pair product of
648 (base pairs 2641 to 3288) for Fprimer2 and Rprimer2 and 838 (base pairs
2641 to 3478) for Fprimer3 and Rprimer3 due to them being able to accurately
anneal to the wild-type or mutant allele of the heterozygous DNA (Zielenski,
1990). The successful development of new c.233dupT annealing primers will allow
physicians and scientists to progress the field of diagnosis and treatment of
rare and understudied CFTR mutations in minorities. Discussion Experiment Summary Cystic
fibrosis (CF) is an autosomal recessive disease caused by the mutation of the
cystic fibrosis transmembrane conductance regulator (CFTR) on chromosome 7
which codes for the CFTR protein that facilitates chloride ion movement through
epithelial cells (Welsh and Smith, 1995). When a mutation is present on the
CFTR gene, the CFTR protein production malfunctions and chloride ion movement
is inhibited (Rowe et al, 2005). This change causes thickened mucus in
lumen and airways negatively impacting various organs within the body such as
the lungs, liver, pancreas, and the small intestine (Welsh and Smith, 1995). In
the case of the frameshift mutation c.233dupT, the CFTR protein is not produced
due to the addition of a thymine at the 233rd base pair on exon 3 which causes
a truncation (Hull et al, 1994). In our experiment, the question
addressed is whether or not designed primers can be used in a PCR assay to
correctly anneal and amplify to the c.233dupT DNA segment and further be used
for diagnosis of the rare mutation through agarose gel electrophoresis. We
hypothesize that primers designed with the Yaku-Bonczyk method for a diagnostic
assay of the c.233dupT CFTR mutation will yield an adequate volume of amplified
base pair products through PCR for diagnosis due to increased annealing
precision by intentional nucleotide mismatches at the 3 end causing there to
be two nucleotide mismatches instead of a single mismatch that Taq polymerase
could skip over (Yaku et al., 2008). Original
Predictions Using the
purified wild-type DNA recovered from a team mates buccal cells and the
c.233dupT heterozygous mutant DNA generously donated from the John Hopkins DNA
Laboratory, MD, we predicted the lengths of amplified base pair products
yielded from the PCR primers used for each DNA sample. Primers were designed
using the Yaku-Bonczyk method where an intentional mismatched nucleotide is
placed at the 3 end to decrease annealing efficiency for a more precise
annealing location (Yaku et al., 2008)
(Dieffenbach et al, 1993). Based on the
hypothesis that the primers will correctly anneal from the mismatch at their 3
end, and based on the locations of the primers on the genome, we predicted base
pair products of 307 bp for the published primers (Fprimer1 & Rprimer1)(Taylor,
et al., 1983), 648 bp for our designed wild-type
primers (Fprimer2 & Rprimer2), and 838 bp for our designed mutant primers
(Fprimer3 & Rprimer3)(Zielenski
Results and
Ultimate Findings
In
order to establish an effective PCR protocol, multiple experiments were run
with variations in the PCR mixture concentrations, temperatures, and times as each
factor greatly affects the annealing capability of the primers to the DNA
template (Garibyan and Avashia, 2013).
In
the first phase of the overall experiment, known Lambda bacteriophage virus
primers and
Once
clear control bands were achieved from Lambda, we moved into the next phase of
our experiment that would also act as a second control. As stated earlier, John
Hopkins provided heterozygous DNA for the PCR of their published primers and
our designed primers. In order to further perfect our PCR protocol before
testing our designed primers, we followed the protocol designed by John Hopkins
as well as their primers to attempt to match their known amplified base pair
product of 307 bp. We utilized the same PCR mixture we developed previously
(see methods for details) but used their PCR protocol for times and
temperatures. Their PCR protocol consisted of a total of 30 cycles with a
change in annealing temperature from 52℃ for the first seven cycles to
68℃ for the remaining 23 cycles and 45 second intervals for each PCR
stage (see methods for specifics). We replicated their protocol for multiple
trials and only observed faint bands beneath the ladders which we predicted
could be attributed to primer dimers (Brownie et al., 1997). Since primer dimers are circumvented most times by
altering the annealing temperature (Brownie et
al., 1997), after a few trials, we decided to alter their published
protocol. We kept their original PCR protocol concerning temperatures and
times, but we changed the annealing temperature to a gradient of a range from
45℃ to 51℃ (from IDT annealing temperature calculator) over five
samples (five samples of wild-type and five of mutant). In these gels, we
observed very faint bands in both the wells and down the gel as we originally
predicted for the heterozygous DNA sample (Figures 5 & 6). Although the
bands were faint in the mutant gel and there is evidence of primer dimer, we
calculated a percent error of just 7.42% for the mutant allele band on the gel.
From these
findings, we can conclude that our amplified base pair predictions were correct
and that the PCR protocol we developed could be used in further research of
primers designed for the c.233dupT mutation. However, until further research is
done, we were not able to support or refute our hypothesis regarding the
Yaku-Bonczyk approach for designing primers.
Future Directions
In
order to be able to support or refute our hypothesis concerning Yaku-Bonczyk
primer design, further experimentation would be required. In future
experiments, we would alter our previous protocol for our published primer gels
by creating a new temperature gradient in order to have more precise bands and
to circumvent the possible primer dimers observed. We observed the most ideal
bands closer to the 51℃ end of the gradient so
the new gradient would be set between the temperatures of 51℃ to
61℃.
Once clear, precise bands are observed on a new agarose
gel, we will move into the final phase of our experiment. We will use the same
PCR protocol developed for the Lambda and published control, but use primers
designed using the Yaku-Bonczyk method. For the wild-type allele of the
heterozygous DNA, we designed a forward primer (Fprimer2) that, at the 3 end,
consists of a cytosine which corresponds to the wild-type allele sequence (5- GCC CTT CGG CGA TGT TTT ATC -3). For the mutant allele
of the heterozygous DNA, we designed a forward primer (Fprimer3) that, at the
3 end, consists of an extra thymine due to the c.233dupT frameshift mutation (5-
GCC CTT CGG CGA TGT TTT ATT -3). The reverse primer for the wild-type allele
(Rprimer2; 5-TTC CTC CTT GTT ATC CGG GTC-3) was designed to anneal at a base
pair location that would yield an amplified base pair product of 648 with
Fprimer2. Conversely, the reverse primer for the mutant allele (Rprimer3; 3-
CCG GGG TAC CGT GTA TAT AAG -5) was designed to yield a base pair product of
838.
With successful amplification of the wild-type and mutant
alleles at the c.233dupT loci verified by a semi-log plot, our hypothesis
concerning the use of the Yaku-Bonczyk primer design method could be supported.
From there, diagnostic assays using our designed primers for the c.233dupT CFTR
mutation could be readily utilized by diagnostic laboratories.
______________________________________________________________________________
Figures
A
B
Figure 6. Agarose
gel electrophoresis resulting from PCR of mutant published primers and
heterozygous mutant DNA for c.233dupT. (A) Agarose gel was run at 200V
for 11 minutes. For the first and eighth well, a mix of 10 ΅l of Kb+ ladder and 2 ΅l of bromophenol blue dye was inserted to
create a visible ladder to use as a point of reference for migration distance
of bands. In the second well, a negative control of 10 ΅l nuclease-free water
and 2 ΅l bromophenol blue dye were inserted. In the third through seventh well,
10 ΅l of the PCR cocktail containing heterozygous mutant DNA and the mutant
primers, along with 2 ΅l of bromophenol blue dye were inserted. As expected,
bands showed up in both the top wells and at 307 base pairs in lanes three
through seven. This result shows that the wild-type allele of the mutant DNA
was not amplified, while the mutant allele of the DNA was amplified due to
successful annealing of the mutant published primers. (B) A semi-log
plot was created in order to calculate the approximate molecular size (base
pair length) of the acquired bands. Ladder values from Invitrogen were used in
comparison to measured band distance from the wells in centimeters, especially
for the 307 base pair band of interest. A power line was used which resulted in
an equation of y=156201x-3.896 and an R2 of 0.97342.