Red queen dynamics and the evolution of translational redundancy and degeneracy

Abstract

We explore adaptive theories for the diversity of protein translation based on the genetic code viewed as a primitive immune system. Immunity is acquired through a genetic mechanism of non-recognition of parasite genomes. 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. Changing the binding specifity can be thought of in terms of varying degrees of redundancy and degeneracy. Redundancy in the genetic code is commonly attributed to using a four base triplet mechanism to encode the 20 amino acids. This has been referred to as synonym redundancy. There are however at least a further two forms of redundancy associated with the code and one source of degeneracy. A first form of redundancy arises from decoding all 61 possible sense codons using fewer than 61 anticodons. Such a strategy involves reduced binding specificity. A second source of redundancy is present in the multiplicity of copies of each unique tRNA (tRNA copy redundancy). Degeneracy arises when different anticodons become associated with a single amino acid to increase specificity. Variation in these strategies across tax a ensures that the translational machinery is diverse whereas the code remains approximately constant.We construct a red queen theory for translational diversity: a theory in which host translational strategies - as defined by the degree of redundancy or degeneracy of anticodons— are constantly shifting through time to evade parasitism but where neither parasite nor host gains a systematic advantage.