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Additionally, it is usual to use degenerate codons that minimise stop codons (which are generally not desired). Consequently, the fully randomised 'NNN' is not ideal, and alternative, more restricted degenerate codons are used. 'NNK' and 'NNS' have the benefit of encoding all 20 amino acids, but still encode a stop codon 3% of the time.
Degeneracy or redundancy [1] of codons is the redundancy of the genetic code, exhibited as the multiplicity of three-base pair codon combinations that specify an amino acid. The degeneracy of the genetic code is what accounts for the existence of synonymous mutations . [ 2 ] :
Codon usage bias in Physcomitrella patens. Codon usage bias refers to differences in the frequency of occurrence of synonymous codons in coding DNA.A codon is a series of three nucleotides (a triplet) that encodes a specific amino acid residue in a polypeptide chain or for the termination of translation (stop codons).
Examples of degeneracy are found in the genetic code, when many different nucleotide sequences encode the same polypeptide; in protein folding, when different polypeptides fold to be structurally and functionally equivalent; in protein functions, when overlapping binding functions and similar catalytic specificities are observed; in metabolism, when multiple, parallel biosynthetic and ...
The stop codon recruits a release factor, terminating translation. On the right is a diagram of the tRNA suppression mechanism where the codon and the tRNA are both mutated, resulting in tRNA suppression. The mutated Tyr tRNA has the anticodon AUC which recognizes the UAG stop codon, continuing protein translation. [9] Nonsense-mediated mRNA decay
The ambush hypothesis is a hypothesis in the field of molecular genetics that suggests that the prevalence of “hidden” or off-frame stop codons in DNA selectively deters off-frame translation of mRNA to save energy, molecular resources, and to reduce strain on biosynthetic machinery by truncating the production of non-functional, potentially cytotoxic protein products. [1]
In the most common variant of sickle-cell disease, the 20th nucleotide of the gene for the beta chain of hemoglobin is altered from the codon GAG to GTG. Thus, the 6th amino acid glutamic acid is substituted by valine —notated as an "E6V" mutation—and the protein is sufficiently altered to cause the sickle-cell disease.
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