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Silent mutations, also called synonymous or samesense mutations, are mutations in DNA that do not have an observable effect on the organism's phenotype. The phrase silent mutation is often used interchangeably with the phrase synonymous mutation ; however, synonymous mutations are not always silent, nor vice versa.
A synonymous mutation can affect transcription, splicing, mRNA transport, and translation, any of which could alter the resulting phenotype, rendering the synonymous mutation non-silent. [3] The substrate specificity of the tRNA to the rare codon can affect the timing of translation, and in turn the co-translational folding of the protein. [1]
A nonsynonymous substitution is a nucleotide mutation that alters the amino acid sequence of a protein.Nonsynonymous substitutions differ from synonymous substitutions, which do not alter amino acid sequences and are (sometimes) silent mutations.
Not all missense mutations lead to appreciable protein changes. An amino acid may be replaced by an amino acid of very similar chemical properties, in which case, the protein may still function normally; this is termed a neutral, "quiet", "silent" or conservative mutation.
The genetic differences among divergent populations can involve silent mutations (that have no effect on the phenotype) or give rise to significant morphological and/or physiological changes. Genetic divergence will always accompany reproductive isolation, either due to novel adaptations via selection and/or due to genetic drift, and is the ...
Mutations are permanent, transmissible changes to the genetic material (usually DNA or RNA) ... Silent mutation; Single-nucleotide polymorphism; Slipped strand ...
Many mutations are silent mutations, causing no visible effects at all, either because they occur in non-coding or non-functional sequences, or they do not change the amino-acid sequence due to the redundancy of codons. [33] Some mutagens can cause aneuploidy and change the number of chromosomes in the cell. They are known as aneuploidogens. [34]
Typically, silent mutations in protein-coding regions are used as the "control" in the McDonald–Kreitman test. In 1991, John H. McDonald and Martin Kreitman derived the McDonald–Kreitman test while performing an experiment with Drosophila (fruit flies) and their differences in amino acid sequence of the alcohol dehydrogenase gene.