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Saturation mutagenesis is commonly achieved by site-directed mutagenesis PCR with a randomised codon in the primers (e.g. SeSaM) [2] or by artificial gene synthesis, with a mixture of synthesis nucleotides used at the codons to be randomised. [3] Different degenerate codons can be used to encode sets of amino acids. [1]
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).
With some exceptions, [1] a three-nucleotide codon in a nucleic acid sequence specifies a single amino acid. The vast majority of genes are encoded with a single scheme (see the RNA codon table ). That scheme is often called the canonical or standard genetic code, or simply the genetic code, though variant codes (such as in mitochondria ) exist.
Early attempts at mutagenesis using radiation or chemical mutagens were non-site-specific, generating random mutations. [2] Analogs of nucleotides and other chemicals were later used to generate localized point mutations, [3] examples of such chemicals are aminopurine, [4] nitrosoguanidine, [5] and bisulfite. [6]
Nirenberg (right) and Matthaei at the National Institutes of Health. The Nirenberg and Matthaei experiment was a scientific experiment performed in May 1961 by Marshall W. Nirenberg and his post-doctoral fellow, J. Heinrich Matthaei, at the National Institutes of Health (NIH).
Effective number of codons (abbreviated as ENC or Nc) is a measure to study the state of codon usage biases in genes and genomes. [1] The way that ENC is computed has obvious similarities to the computation of effective population size in population genetics. [2]
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