Variant codes are alterations affecting all proteins of the organisms or organelles, with redistribution of the preexisting degeneracy. No case is known of full loss of any of the attributions, so that the standard configuration of the code is preserved, and our model survives also this test. The general mechanism is of a decoding system developing expanded capability (most frequently due to posttranscriptional modification of tRNAs, that become able to decode new codons, plus their acceptance by the synthetases, or ribosomal changes), substituting the previous meaning of one or more codons (the donor codons). The variants are considered to have developed after the standard code was formed, due to being dependent on changes in various components of the decoding system, which require complex genomes, containing sets of tRNA-modifying enzymes, besides ribosomes and the aRS sets. In each type or occurrence of a change, the expansion of the decoding system may be preceded or followed by the loss of the former meaning of the donor codon. When it is preceded by the loss of a codon (e.g. in genomes with strongly biased base compositions, such as in the mitochondria and in the firmicute bacteria) or of its meaning (e.g. loss of tRNA-modifying enzymes), it may be said that the expansion is an event of compensation for the loss. Genomic minimization or simplification is also indicated to be a causal mechanism, evidenced in mitochondria and in the firmicute-derived mycoplasmas.
It is indicated that the changes observed (see Guimaraes et al., 2007) were those that could be tolerated, occurring upon attributions that are more expendable and less crucial to physiology. Attributions not tolerating losses, that became essential to all organisms and organelles, are in three of the complex boxes (Phe, [Leu]; His, Gln; Asp, Glu) and in the five simple boxes of the nonhexacodonic attributions (Pro, Gly, Val, Ala, Thr). The high prevalence of changes in the punctuation boxes is possibly due to the complexity and plasticity of the punctuation mechanisms, involving the protein factors. The high frequency of changes in the box containing the dicodonic components of the hexacodonics Ser and [Arg] indicates that these attributions are less crucial to physiology and more expendable than other codes.
We indicate that the functional hierarchy corresponds to a temporal hierarchy: attributions fixed earlier became more tightly integrated to other components of the physiological network (as hubs), and therefore more difficult to change. The later attributions would be more loosely coupled to the network, therefore more expendable. The more widely connected earlier attributions would be also more apt for adopting extra codes. Evidences for the physiological and temporal hierarchy are: (a) The vast majority of the donors are the 5 R codonic attributions; there are only two losses of 5' Y codons (AGY Ser). Such instability of the 5' codons (or 5' Y anticodons) may be among the forces resulting in the maintenance of the two types of 5' bases in the cellular anticodes. (b) Stop codons changed most frequently to amino acid attributions, there being only two occurrences of the reverse path (AGR [Arg] or UCA Ser changing to Stop). (c) Codons with 5' R changed to the 5' Y meanings (UGA Stop to Cys, UAA Stop to Tyr, AGR [Arg] to Ser, AAA Lys to Asn), there being no example of the reverse path. (d) There are also changes between the 5' Y (UGA Stop to Trp, the AUA exchanges between Ile and Met). (e) Other examples of changes between different boxes are also from late fixations conceding to earlier ones (AGR [Arg] to Gly, AGY Ser to Gly, CUG Leu to Ser), there being one example of the reverse path (CUN Leu to Thr). The general panorama of the changes can be interpreted as loss of complexity of the matrix or reversal to simpler or earlier states.
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