Codon Table

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The standard codon table is given below.

UUU F/Phe Phenylalanine UCU S/Ser Serine UAU Y/Tyr Tyrosine UGU C/Cys Cysteine
UUC UCC UAC UGC
UUA L/Leu Leucine UCA UAA * Ochre Stop UGA * Opal Stop
UUG UCG UAG * Amber Stop UGG W/Trp Tryptophan
CUU CCU P/Pro Proline CAU H/His Histidine CGU R/Arg Arginine
CUC CCC CAC CGC
CUA CCA CAA Q/Gln Glutamine CGA
CUG CCG CAG CGG
AUU I/Ile Isoleucine ACU T/Thr Threonine AAU N/Asn Asparagine AGU S/Ser Serine
AUC ACC AAC AGC
AUA ACA AAA K/Lys Lysine AGA R/Arg Arginine
AUG M/Met Methionine ACG AAG AGG
GUU V/Val Valine GCU A/Ala Alanine GAU D/Asp Aspartic acid GGU G/Gly Glycine
GUC GCC GAC GGC
GUA GCA GAA E/Glu Glutamic acid GGA
GUG GCG GAG GGG

Cells are colored fro the amino acid from hydrophobic (blue) to hydrophilic (red) according to the order given in Lenstra 2015 and the HTML color code gradient (inverse HSV Gradient) was generated from http://www.perbang.dk/rgbgradient/.

DNA sequences are transcribed into mRNA by RNA polymerase II.

Codons that code for amino acids on the mRNA are recognized by tRNA's which are used by the Ribosome to produce polypeptides.

The codon table is not universal. However, variants are similar to the standard table with very few changes. Many of the known variants are mitochondrial which has a small genome and is possibly more likely to undergo stochastic codon changes.

Bacteria and phages can use alternative tables to defend against infection or to promote viral replication.

Release Factors

Stop codons are not recognized by tRNA's. Release Factors are proteins that recognize the stop codons.

In Eukaryotes RF1 recognizes all three stop codons. In Prokaryotes Release Factor 1 (RF1) recognizes amber UAG and ochre UAA and RF2 recognizes ochre UAA and opal UGA.

An excellent example of the evolution of bacterial and viral codons, where the bacteria initially recodes a stop codon to interfere with phage translation but the phage evolves to accommodate this and interfere with bacterial translation, is given in Ivanova et al. 2014. Bacteria in the human mouth are enriched for UGA (opal) recoded bacteria lacking RF2 but containing RF1 that recognizes UAG and UAA stop codons. A virus, phage 2, has been described that produces its own RF2 and reassigned UAG tRNA. Genes that are needed early in infection and invasion as well as RF2 avoid UAG because this would be mistranslated by the bacterial cell and not produce the correct polypeptides required by the virus. As the infection proceeds the viral RF2 terminates bacterial genes prematurely at UGA sites because they are now beginning to be recognized as stop codons. The viral UAG tRNA also interferes with bacterial protein sequences. This disrupts the bacteria and also blocks RF1 production. Genes that are required later in infection, virus assembly, and cell lysis contain UAG that are not recognized as an amino acid because of the lack of bacterial RF1. They are also correctly terminated at UAA and UGA stop codons by the viral RF2.

Links

https://www.nature.com/scitable/blog/bio2.0/battle_of_the_genetic_codes

http://science.sciencemag.org/content/344/6186/909

http://phenomena.nationalgeographic.com/2013/10/17/find-and-replace-across-an-entire-genome/

https://www.usnews.com/news/news/articles/2017-07-26/how-scientists-redesign-dna-codes