Abstract
We explore adaptive theories for the diversity of translational binding based on the genetic code viewed as a primitive mechanism of resistance. Modifying the set of codons bound by tRNA anticodon molecules or changing the specificity of binding, reduces the replication rate of translational parasites such as viruses. Increased translational efficiency of the parasite requires a high degree of specificity of host tRNAs for the parasite codons. This suggests that the genetic code might serve as the first line of defense against infection. We construct a red queen theory for translational diversity: a theory in which host-translational strategies— as defined by the degree of redundancy (a single anticodon binding many codons for a single amino acid) or degeneracy (many anticodons binding many codons for a single amino acid)—are constantly shifting through time to evade parasitism but where neither parasite nor host gain a systematic advantage.
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