490:
translation. This is an example of how some silent mutations are not always silent. The multi-drug resistance genes at Exon 26 C3435T, exon 21 G2677T/A, and exon 12 C1236T have been studied to have SNP's that occur at the same time, therefore making the phenotypic "function "change. This suggests a haplotype dependency between exon 26 and other exon that have polymorphisms. For example, efavirenz and nelfinavir are two types of drugs that help decrease the HIV infection in a person's body. When the SNP from exon 26 is coupled with other SNP exons, the drugs have a lower chance of maintaining the HIV infection. Although, when the TT nucleotides in exon 26 are expressed the patient has a lower concentration of the virus but when the genotype morphs into CC or CT the infection is able to spread like normal leaving the MDR 1 gene almost defenseless. These changes in bases of exon 26 for MDR 1 show a correlation between the MDR 1 gene mutations and the ability of the antiretroviral drugs to suppress the HIV infection.
494:
of exon 26’s haplotype dependency is seen when looking at chemotherapy. Since MDR 1 removes drugs from our cells, inhibitors have been used to block MRD 1's ability to remove drugs, thus letting beneficial drugs like chemotherapy and immunosuppressants aid the body in recovery more efficiently. MDR1 has different proteins that help exile these specific drugs from cancer cells. Verapamil and cyclosporine A are common inhibitors for MDR 1. Unfortunately, when C3435T is mutated with a mutation from either exon 12 or exon 21 (or if all three mutations occur at the same time creating a haplotype), the inhibitors are less likely to weaken the function of MDR1. Multiple silent mutated genes tend to be more resistant against these inhibitors.
266:
could refold into the native tertiary form. The tertiary structure of a protein is a fully folded polypeptide chain with all hydrophobic R-groups folded into the interior of the protein to maximize entropy with interactions between secondary structures such as beta sheets and alpha helixes. Since the structure of proteins determines its function, it is critical that a protein be folded correctly into its tertiary form so that the protein will function properly. However, it is important to note that polypeptide chains may differ vastly in primary structure, but be very similar in tertiary structure and protein function.
486:
MDR1 codes for the P-glycoprotein which helps get rid of drugs in the body. It is located in the intestines, liver, pancreas, and brain. MDR 1 is located in the same places that CYP3A4 is located in, which is an enzyme that helps get rid of toxins or drugs from the liver and intestines. Silent mutations like MDR 1 do express a change in phenotypic response. A study done on mice showed when they did not have enough of the MDR 1 gene, their body did not recognize the ivermectin or cyclosporine drug, leading to the creation of toxins in their bodies.
316:
structure is maintained by dinucleotide relative abundances in the cell matrix. It has also been discovered that mRNA secondary structure is important for cell processes such as transcript stability and translation. The general idea is that the functional domains of mRNA fold upon each other, while the start and stop codon regions generally are more relaxed, which could aid in the signaling of initiation and termination in translation.
31:
498:
when exon 26 changes ATC to ATT both codons produce the same amino acid but ATC is seen more often than the mutation codon. As a consequence, the amount of time it takes for the ribosome to produce its protein confirmation is changed. This leads to a protein structure different from the usual shape of the protein which leads to different functions of the protein.
350:
on the favored specific tertiary structure because of other competing structures. RNA-binding proteins can assist RNA folding problems, however, when a silent mutation occurs in the mRNA chain, these chaperones do not bind properly to the molecule and are unable to redirect the mRNA into the correct fold.
493:
Exon 26 has also been studied as to whether it is haplotype dependent or not. The presence of the SNP of exon 26 changes phenotypic functions when it is paired with the presence of mutations from exons 12 and 21. But when acting alone, it does not affect the phenotypic outcome as strongly. An example
238:
refers to its amino acid sequence. A substitution of one amino acid for another can impair protein function and tertiary structure, however its effects may be minimal or tolerated depending on how closely the properties of the amino acids involved in the swap correlate. The premature insertion of a
501:
Other reasons behind MDR1’s “silent mutation” occurs in messenger RNA. In mRNA, codons also work as exon splicing enhancers. Codons decide when to cut out introns based on the codon it is reading in mRNA. The mutated codons have a higher risk of making a mistake when splicing introns out of the mRNA
497:
Looking at the molecular level, the reason why C3435T in exon 26 of MDR 1 gene is not silent is because of the pace at which the amino acids are being translated to proteins. mRNA’s secondary structures can fold which means different codons correspond to different folding's of the mRNA. For example,
300:
amino acid residue. The other common type of secondary structure is the beta sheet, which displays a right-handed twist, can be parallel or anti-parallel depending on the direction of the direction of the bonded polypeptides, and consists of hydrogen bonds between the carbonyl and amino groups
485:
Around 99.8% of genes that undergo mutations are deemed silent because the nucleotide change does not change the amino acid being translated. Although silent mutations are not supposed to have an effect on the phenotypic outcome, some mutations prove otherwise like the Multi-Drug
Resistance Gene 1.
349:
Silent mutations affect protein folding and function. Normally a misfolded protein can be refolded with the help of molecular chaperones. RNA typically produces two common misfolded proteins by tending to fold together and become stuck in different conformations and it has a difficulty singling in
265:
Furthermore, a change in primary structure is critical because the fully folded tertiary structure of a protein is dependent upon the primary structure. The discovery was made throughout a series of experiments in the 1960s that discovered that reduced and denatured RNase in its unfolded form
315:
Furthermore, since all organisms contain a slightly different genetic code, their mRNA structures differ slightly as well, however, multiple studies have been conducted that show that all properly folded mRNA structures are dependent on the primary sequence of the polypeptide chain and that the
163:
are passed from the parent to the offspring. Scientists have predicted that people have approximately 5 to 10 deadly mutations in their genomes but this is essentially harmless because there is usually only one copy of a particular bad gene so diseases are unlikely. Silent mutations can also be
376:
in which the virus was engineered to have synonymous codons replace naturally occurring ones in the genome. As a result, the virus was still able to infect and reproduce, albeit more slowly. Mice that were vaccinated with this vaccine and exhibited resistance against the natural polio strain.
123:
The genetic code translates mRNA nucleotide sequences to amino acid sequences. Genetic information is coded using this process with groups of three nucleotides along the mRNA which are commonly known as codons. The set of three nucleotides almost always produce the same amino acid with a few
489:
MRD1 has over fifty single nucleotide polymorphisms (SNP's) which are changes in the nucleotide base sequence. In MDR1 the gene exon 26 which represents 3535C can mutate to 3535T which then changes the transfer RNA into one that is not often as seen, leading to changes in the outcome during
214:
will be carried out at a much slower rate. This can result in lower expression of a particular gene containing that silent mutation if the mutation occurs within an exon. Additionally, if the ribosome has to wait too long to receive the amino acid, the ribosome could terminate translation
307:
has a secondary structure that is not necessarily linear like that of DNA, thus the shape that accompanies complementary bonding in the structure can have significant effects. For example, if the mRNA molecule is relatively unstable, then it can be rapidly degraded by enzymes in the
291:
Secondary structure of proteins consists of interactions between the atoms of the backbone of a polypeptide chain, excluding the R-groups. One common type of secondary structures is the alpha helix, which is a right-handed helix that results from hydrogen bonds between the
413:). These two mutations are both shared by the low pain sensitivity and high pain sensitivity gene. Low pain sensitivity has an additional CTC to CTG silent mutation, while high pain sensitivity does not and shares the CTC sequence at this location with average pain sensitivity.
247:, can alter the primary structure of a protein. In this case, a truncated protein is produced. Protein function and folding is dependent on the position in which the stop codon was inserted and the amount and composition of the sequence lost.
144:–different codons result in the same amino acid. Codons that code for the same amino acid are termed synonyms. Silent mutations are base substitutions that result in no change of the amino acid or amino acid functionality when the altered
402:), which codes for a cellular membrane pump that expels drugs from the cell, can slow down translation in a specific location to allow the peptide chain to bend into an unusual conformation. Thus, the mutant pump is less functional.
502:
sequence leading to the wrong exons being produced. Therefore, making a change to the mature messenger RNA. Mutations in the Multi-Drug
Resistance Gene 1 show how silent mutations can have an effect on the outcome of the phenotype.
261:
Historically, silent mutations were thought to be of little to no significance. However, recent research suggests that such alterations to the triplet code do affect protein translation efficiency and protein folding and function.
1653:
By large-scale computer-aided redesign of the viral genome we engineered hundreds of silent mutations into poliovirus. ... We termed this process of perturbing intrinsic viral genome biases by synthetic genome re-design SAVE for
353:
Recent research suggests that silent mutations can have an effect on subsequent protein structure and activity. The timing and rate of protein folding can be altered, which can lead to functional impairments.
312:. If the RNA molecule is highly stable, and the complementary bonds are strong and resistant to unpacking prior to translation, then the gene may be under expressed. Codon usage influences mRNA stability.
198:
There is a different tRNA molecule for each codon. For example, there is a specific tRNA molecule for the codon UCU and another specific for the codon UCC, both of which code for the amino acid
250:
Conversely, silent mutations are mutations in which the amino acid sequence is not altered. Silent mutations lead to a change of one of the letters in the triplet code that represents a
234:
A nonsynonymous mutation that occurs at the genomic or transcriptional levels is one that results in an alteration to the amino acid sequence in the protein product. A protein's
1062:
Czech A, Fedyunin I, Zhang G, Ignatova Z (October 2010). "Silent mutations in sight: co-variations in tRNA abundance as a key to unravel consequences of silent mutations".
159:
Mutations are often linked to diseases or negative impacts but silent mutations can be extremely beneficial in creating genetic diversity among species in a population.
319:
If the oncoming ribosome pauses because of a knot in the RNA, then the polypeptide could potentially have enough time to fold into a non-native structure before the
1132:
206:
into a polypeptide chain would happen a thousand times more slowly when a mutation causes the codon to change from UCU to UCC. If amino acid transport to the
103:) are often classified as silent; if the properties of the amino acid are conserved, this mutation does not usually significantly affect protein function.
254:, but despite the single base change, the amino acid that is coded for remains unchanged or similar in biochemical properties. This is permitted by the
1149:
864:
2099:
1759:
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experiments, it can be useful to introduce silent mutations into a gene of interest in order to create or remove recognition sites for
1799:
1038:
815:
180:
623:
Chamary JV, Parmley JL, Hurst LD (February 2006). "Hearing silence: non-neutral evolution at synonymous sites in mammals".
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17:
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can affect the timing of translation, and in turn the co-translational folding of the protein. This is reflected in the
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75:, any of which could alter phenotype, rendering the synonymous mutation non-silent. The substrate specificity of the
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275:
195:(tRNA) availability is one of the reasons that silent mutations might not be as silent as conventionally believed.
344:
229:
1400:
Montera M, Piaggio F, Marchese C, Gismondi V, Stella A, Resta N, Varesco L, Guanti G, Mareni C (December 2001).
1615:"Putting synthesis into biology: a viral view of genetic engineering through de novo gene and genome synthesis"
255:
1686:
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1745:
202:. In this instance, if there was a thousand times less UCC tRNA than UCU tRNA, then the incorporation of
1524:
770:
59:; however, synonymous mutations are not always silent, nor vice versa. Synonymous mutations can affect
2078:
1886:
406:
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1553:
1240:
874:
362:
Silent mutations have been employed as an experimental strategy and can have clinical implications.
148:(mRNA) is translated. For example, if the codon AAA is altered to become AAG, the same amino acid –
1719:"WatCut: An on-line tool for restriction analysis, silent mutation scanning, and SNP-RFLP analysis"
332:
60:
566:
Kimchi-Sarfaty C, Oh JM, Kim IW, Sauna ZE, Calcagno AM, Ambudkar SV, Gottesman MM (January 2007).
2109:
2073:
1881:
1825:
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410:
179:
Because silent mutations do not alter protein function they are often treated as though they are
1331:
1912:
1402:"A silent mutation in exon 14 of the APC gene is associated with exon skipping in a FAP family"
1235:
805:
2033:
1997:
1960:
1804:
1789:
521:
211:
72:
1942:
1794:
978:
967:"Modeling effects of human single nucleotide polymorphisms on protein-protein interactions"
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8:
2007:
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that is observed in many species. Mutations that cause the altered codon to produce an
34:
Point substitution mutations of a codon, classified by their impact on protein sequence
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Deviations from average pain sensitivity are caused by both an ATG to GTG mutation (
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2012:
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Mental disorders can be caused by silent mutations. One silent mutation causes the
184:
84:
80:
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1809:
736:
365:
1979:
990:
536:
480:
399:
1110:
1097:
Komar AA (August 2007). "Silent SNPs: impact on gene function and phenotype".
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for the use of particular codons due to the need for translational stability.
49:
that do not have an observable effect on the organism's phenotype. The phrase
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1845:
1250:
1223:
173:
145:
133:
1299:
1282:
1175:"A periodic pattern of mRNA secondary structure created by the genetic code"
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1955:
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1308:
1208:
1118:
1083:
1048:
1008:
951:
933:
755:
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192:
137:
136:. Most amino acids are specified by multiple codons demonstrating that the
118:
112:
1722:
1417:
1367:
1259:
1840:
1190:
712:"Non-silent story on synonymous sites in voltage-gated ion channel genes"
568:"A "silent" polymorphism in the MDR1 gene changes substrate specificity"
324:
240:
129:
125:
100:
88:
1737:
1075:
918:"Codon usage: nature's roadmap to expression and folding of proteins"
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gene to be less stable and degrade faster, underexpressing the gene.
309:
30:
687:
670:
636:
567:
1928:
804:
Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P (2007).
207:
42:
1133:"MIT Biochemistry Lecture Notes-Protein Folding and Human Disease"
1548:
1546:
381:
153:
96:
27:
DNA mutation with no observable effect on an organism's phenotype
203:
199:
149:
1543:
1399:
1351:"Analyzing effects of naturally occurring missense mutations"
710:
Zhou T, Ko EA, Gu W, Lim I, Bang H, Ko JH (31 October 2012).
373:
251:
1897:
1172:
320:
304:
285:
76:
68:
1061:
892:(6th ed.). San Francisco: Pearson/Benjamin Cummings.
46:
1721:. University of Waterloo. April 17, 2014. Archived from
964:
565:
803:
398:
A silent mutation in the multidrug resistance gene 1 (
1348:
965:
Teng S, Madej T, Panchenko A, Alexov E (March 2009).
357:
1612:
1581:Campbell, Mary K.; Farrell, Shawn O. (2011-01-01).
622:
1355:Computational and Mathematical Methods in Medicine
1026:
124:exceptions like UGA which typically serves as the
1173:Shabalina SA, Ogurtsov AY, Spiridonov NA (2006).
276:Biomolecular structure § Secondary structure
2091:
345:Biomolecular structure § Tertiary structure
1580:
1020:
1018:
911:
909:
474:
230:Biomolecular structure § Primary structure
1613:Mueller S, Coleman JR, Wimmer E (March 2009).
561:
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53:is often used interchangeably with the phrase
1913:
1753:
1488:
1486:
1349:Zhang Z, Miteva MA, Wang L, Alexov E (2012).
1684:
1522:
1342:
1224:"RNA chaperones and the RNA folding problem"
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301:of the backbone of two polypeptide chains.
1920:
1906:
1760:
1746:
1523:Strachan, Tom; Read, Andrew (2018-03-29).
1483:
1283:"Genetics. SNPs, silent but not invisible"
671:"Synonymous mutations break their silence"
218:
1687:"How Trivial DNA Changes Can Hurt Health"
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1249:
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368:at the Stony Brook University designed a
2047:Mutation with respect to overall fitness
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1513:
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1454:
1452:
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29:
1767:
1329:
835:
778:Nature Encyclopedia of the Human Genome
14:
2092:
887:
799:
797:
668:
269:
183:. Many organisms are known to exhibit
1901:
1741:
1499:. Lippincott Williams & Wilkins.
1496:High-yield Cell and Molecular Biology
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1462:
1447:
1280:
1096:
915:
768:
338:
859:
857:
831:
829:
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327:. Silent mutations may also affect
223:
2100:Modification of genetic information
1228:The Journal of Biological Chemistry
794:
24:
1972:Mutation with respect to structure
1605:
358:Research and clinical applications
25:
2121:
1831:Models of nucleotide substitution
1703:10.1038/scientificamerican0609-46
1685:Chamary J, Hurst LD (June 2009).
1677:
854:
838:Genetics: Analysis and Principles
824:
1554:"The Sound of a Silent Mutation"
1469:. Oxford University Press, USA.
1332:"The Sound of a Silent Mutation"
840:. McGraw-Hill Higher Education.
810:. Garland Science. p. 264.
152:– will be incorporated into the
1393:
1323:
1274:
1215:
1166:
1142:
1125:
106:
1631:10.1016/j.chembiol.2009.03.002
1222:Herschlag D (September 1995).
881:
762:
703:
616:
409:), and a CAT to CAC mutation (
256:degeneracy of the genetic code
13:
1:
1463:Weber, Wendell (2008-04-02).
1150:"Orders of protein structure"
890:Molecular Biology of the Gene
807:Molecular Biology of the Cell
547:
172:, which cause a shift in the
1927:
1330:Beckman (22 December 2006).
1033:(2nd ed.). Wiley-Liss.
1025:Strachan T, Read AP (1999).
737:10.1371/journal.pone.0048541
475:Multi-Drug Resistance Gene 1
91:with similar functionality (
7:
1406:Journal of Medical Genetics
505:
296:amino acid residue and the
280:Silent mutations alter the
187:, suggesting that there is
10:
2126:
2029:Chromosomal translocations
1887:Nonsynonymous substitution
991:10.1016/j.bpj.2008.12.3904
669:Goymer P (February 2007).
478:
342:
273:
227:
116:
110:
2046:
2021:
1978:
1971:
1935:
1859:
1818:
1775:
1493:Dudek, Ronald W. (2007).
1281:Komar AA (January 2007).
1111:10.2217/14622416.8.8.1075
323:molecule can add another
1526:Human Molecular Genetics
1251:10.1074/jbc.270.36.20871
1029:Human Molecular Genetics
836:Brooker R (2017-02-01).
625:Nature Reviews. Genetics
2069:Nearly neutral mutation
1882:Synonymous substitution
1826:Models of DNA evolution
1619:Chemistry & Biology
1300:10.1126/science.1138239
865:"Mutations and Disease"
675:Nature Reviews Genetics
593:10.1126/science.1135308
542:Synonymous substitution
333:transcriptional control
219:Structural consequences
2079:Nonsynonymous mutation
2034:Chromosomal inversions
1936:Mechanisms of mutation
1179:Nucleic Acids Research
934:10.1002/biot.201000332
776:. In Cooper DN (ed.).
771:"Single Base Mutation"
181:evolutionarily neutral
35:
2059:Advantageous mutation
1998:Conservative mutation
1805:Stabilizing selection
1790:Directional selection
1418:10.1136/jmg.38.12.863
922:Biotechnology Journal
916:Angov E (June 2011).
522:Genealogical DNA test
117:Further information:
95:a mutation producing
33:
2054:Deleterious mutation
2022:Large-scale mutation
1795:Disruptive selection
1587:. Cengage Learning.
1064:Molecular BioSystems
870:The Tech Interactive
393:dopamine receptor D2
128:but can also encode
2074:Synonymous mutation
2008:Frameshift mutation
1860:Molecular processes
1785:Balancing selection
1769:Molecular evolution
1691:Scientific American
1683:Overview article —
1529:. Garland Science.
1368:10.1155/2012/805827
983:2009BpJ....96.2178T
971:Biophysical Journal
728:2012PLoSO...748541Z
584:2007Sci...315..525K
386:restriction enzymes
282:secondary structure
270:Secondary structure
161:Germ-line mutations
56:synonymous mutation
18:Silent substitution
1800:Negative selection
1191:10.1093/nar/gkl287
888:Watson JD (2008).
339:Tertiary structure
185:codon usage biases
36:
2087:
2086:
2042:
2041:
1993:Missense mutation
1988:Nonsense mutation
1895:
1894:
1777:Natural selection
1040:978-1-85996-202-2
817:978-1-136-84442-3
532:Nonsense mutation
527:Missense mutation
472:
471:
245:nonsense mutation
236:primary structure
224:Primary structure
16:(Redirected from
2117:
2064:Neutral mutation
2013:Dynamic mutation
1976:
1975:
1922:
1915:
1908:
1899:
1898:
1872:Gene duplication
1836:Allele frequency
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1466:Pharmacogenetics
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1099:Pharmacogenomics
1094:
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1076:10.1039/c004796c
1059:
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1032:
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1013:
1012:
1002:
962:
956:
955:
945:
913:
904:
903:
885:
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878:
873:. Archived from
861:
852:
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822:
821:
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792:
791:
775:
769:Graur D (2003).
766:
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749:
739:
707:
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666:
657:
656:
620:
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517:Neutral mutation
512:Codon degeneracy
416:
415:
85:codon usage bias
39:Silent mutations
21:
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2119:
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2116:
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2090:
2089:
2088:
2083:
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2017:
2003:Silent mutation
1967:
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1877:Silent mutation
1867:Gene conversion
1855:
1814:
1810:Selective sweep
1771:
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1606:Further reading
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1347:
1343:
1338:. Science/AAAS.
1328:
1324:
1293:(5811): 466–7.
1279:
1275:
1241:10.1.1.328.5762
1234:(36): 20871–4.
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1147:
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1070:(10): 1767–72.
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773:
767:
763:
708:
704:
688:10.1038/nrg2056
667:
660:
637:10.1038/nrg1770
621:
617:
578:(5811): 525–8.
564:
555:
550:
508:
483:
477:
366:Steffen Mueller
360:
347:
341:
278:
272:
232:
226:
221:
121:
115:
109:
71:transport, and
51:silent mutation
28:
23:
22:
15:
12:
11:
5:
2123:
2113:
2112:
2110:Neutral theory
2107:
2102:
2085:
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2031:
2025:
2023:
2019:
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2010:
2005:
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1995:
1990:
1984:
1982:
1980:Point mutation
1973:
1969:
1968:
1966:
1965:
1964:
1963:
1958:
1950:
1945:
1939:
1937:
1933:
1932:
1925:
1924:
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1889:
1884:
1879:
1874:
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1861:
1857:
1856:
1854:
1853:
1851:Fay and Wu's H
1848:
1843:
1838:
1833:
1828:
1822:
1820:
1816:
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1813:
1812:
1807:
1802:
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1725:on May 4, 2020
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1678:External links
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1558:Science | AAAS
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977:(6): 2178–88.
957:
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899:978-0805395921
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880:
877:on 2022-01-18.
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1412:(12): 863–7.
1411:
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847:9781259616020
843:
839:
832:
830:
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819:
813:
809:
808:
800:
798:
789:
783:
780:. MacMillan.
779:
772:
765:
757:
753:
748:
743:
738:
733:
729:
725:
721:
717:
713:
706:
698:
694:
689:
684:
680:
676:
672:
665:
663:
654:
650:
646:
642:
638:
634:
631:(2): 98–108.
630:
626:
619:
611:
607:
603:
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594:
589:
585:
581:
577:
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569:
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421:
418:
417:
414:
412:
408:
407:nonsynonymous
403:
401:
396:
394:
389:
387:
383:
380:In molecular
378:
375:
371:
367:
363:
355:
351:
346:
336:
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317:
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257:
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248:
246:
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237:
231:
216:
215:prematurely.
213:
209:
205:
201:
196:
194:
190:
186:
182:
177:
175:
174:reading frame
171:
167:
162:
157:
155:
151:
147:
146:messenger RNA
143:
139:
135:
132:in mammalian
131:
127:
120:
114:
104:
102:
98:
94:
90:
86:
82:
78:
74:
70:
66:
62:
61:transcription
58:
57:
52:
48:
44:
40:
32:
19:
2002:
1956:Transversion
1876:
1729:November 22,
1727:. Retrieved
1723:the original
1697:(6): 46–53.
1694:
1690:
1667:
1663:
1659:
1655:
1652:
1622:
1618:
1584:Biochemistry
1583:
1562:. Retrieved
1560:. 2006-12-22
1557:
1525:
1495:
1465:
1440:
1409:
1405:
1395:
1358:
1354:
1344:
1335:
1325:
1290:
1286:
1276:
1231:
1227:
1217:
1182:
1178:
1168:
1157:. Retrieved
1154:Khan Academy
1153:
1144:
1127:
1102:
1098:
1092:
1067:
1063:
1057:
1028:
974:
970:
960:
928:(6): 650–9.
925:
921:
889:
883:
875:the original
868:
837:
806:
777:
764:
719:
715:
705:
678:
674:
628:
624:
618:
575:
571:
500:
496:
492:
488:
484:
466:
458:
445:
438:
430:
404:
397:
390:
379:
370:live vaccine
364:
361:
352:
348:
318:
314:
303:
297:
293:
290:
279:
264:
260:
249:
233:
210:is delayed,
197:
193:Transfer RNA
178:
164:produced by
158:
138:genetic code
134:mitochondria
122:
119:Transfer RNA
113:Genetic code
107:Genetic code
92:
79:to the rare
54:
50:
38:
37:
1841:Ka/Ks ratio
212:translation
99:instead of
73:translation
2094:Categories
1961:Transition
1846:Tajima's D
1670:ngineering
1662:ttenuated
1564:2018-11-18
1159:2018-11-08
1051:. NBK7580.
548:References
411:synonymous
325:amino acid
241:stop codon
166:insertions
142:degenerate
130:tryptophan
126:stop codon
101:isoleucine
89:amino acid
1943:Insertion
1658:ynthetic
1442:Full text
1236:CiteSeerX
681:(2): 92.
310:cytoplasm
189:selection
170:deletions
43:mutations
2105:Mutation
1948:Deletion
1929:Mutation
1711:19485088
1649:19318214
1436:11768390
1387:22577471
1361:: 1–15.
1317:41904137
1309:17185559
1268:14083129
1209:16682450
1119:17716239
1084:20617253
1049:21089233
1009:19289044
952:21567958
756:23119053
716:PLOS ONE
697:29882152
653:25713689
645:16418745
610:15146955
602:17185560
506:See also
329:splicing
208:ribosome
156:chain.
65:splicing
1640:2728443
1427:1734788
1378:3346971
1287:Science
1260:7545662
1200:1458515
1000:2717281
979:Bibcode
943:3166658
747:3485311
724:Bibcode
580:Bibcode
572:Science
382:cloning
154:peptide
97:leucine
1819:Models
1709:
1647:
1637:
1591:
1533:
1503:
1473:
1434:
1424:
1385:
1375:
1315:
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997:
950:
940:
896:
844:
814:
784:
754:
744:
695:
651:
643:
608:
600:
204:serine
200:serine
150:lysine
1666:irus
1313:S2CID
1264:S2CID
1136:(PDF)
774:(PDF)
693:S2CID
649:S2CID
606:S2CID
374:polio
331:, or
298:n+4th
252:codon
81:codon
1731:2014
1707:PMID
1645:PMID
1589:ISBN
1531:ISBN
1501:ISBN
1471:ISBN
1432:PMID
1383:PMID
1359:2012
1336:News
1305:PMID
1256:PMID
1205:PMID
1115:PMID
1080:PMID
1045:PMID
1035:ISBN
1005:PMID
948:PMID
894:ISBN
842:ISBN
812:ISBN
782:ISBN
752:PMID
641:PMID
598:PMID
463:ATG
453:CTC
450:CTC
435:CAT
425:HPS
422:APS
419:LPS
400:MDR1
372:for
321:tRNA
305:mRNA
286:mRNA
243:, a
93:e.g.
77:tRNA
69:mRNA
41:are
1699:doi
1695:300
1635:PMC
1627:doi
1422:PMC
1414:doi
1373:PMC
1363:doi
1295:doi
1291:315
1246:doi
1232:270
1195:PMC
1187:doi
1107:doi
1072:doi
995:PMC
987:doi
938:PMC
930:doi
742:PMC
732:doi
683:doi
633:doi
588:doi
576:315
467:GTG
459:GTG
446:CTG
439:CAC
431:CAC
294:nth
284:of
168:or
140:is
47:DNA
45:in
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