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In E. coli, there are only 47 different tRNAs but 61 potential anticodons. This is because, from what I understand, the third base of the anticodon can pair by wobble rules.

However, it is known that there is some correlation between tRNA pools and expression levels.

So if, for example, GUA and GUG were covered by the same tRNA, why are their codon usages different in a codon table? If one were only concerned with expression level, shouldn't they theoretically affect translation rates similarly?

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This is a good question as, although in higher eukaroyotes codon usage does not necessarily correlate with translational efficiency, it does to a large extent in Escherichia coli (see e.g. Boël et al., 2016). The answer is not simple, but the following may contribute.

To optimize the strength of base pairing

Although in particular circumstances ‘wobble’ allows one tRNA to decode more than one codon (see diagram in my answer to Redundancy and the Generic Code) the strength of base pairing will be less for the wobble base-pair: Comparison of wobble and non-wobble base pairs It has been suggested this would generally disfavour (and hence reduce the incidence of) the degenerate codon that needs to be decoded by wobble. (In some cases a wobble interaction might be an advantage if the first two codon bases were G or C, so that the hydrogen bonding was not too strong.)

To utilize the spectrum of tRNAs able to decode degenerate codons

Although wobble enables a reduction in the total number of tRNAs necessary to decode the 61 amino-acid codons, additional tRNAs often exist that one might regard as unnecessary. Furthermore, where three codons are decoded by a tRNA with a 5'-I (inosine), the other tRNA sometimes has a 5'-G (rather than A) and can hence decode two codons. This is illustrated by the E.coli tRNAs for threonine: tRNAs for degenerate Threonine codons Thus, the relative abundance of these three Thr-tRNAs could determine the codon usage, and Dong et al., 1996 reported that this is the case.

To reflect the overall GC-content of the genome

If the genome of a prokaryotic organism has a particular base composition, because there is so little non-coding genomic DNA the mRNA will necessarily reflect that base composition in its codon usage. Your might ask why doesn’t the base-composition of the genome just reflect that of the synonymous codons, but there are actually strong pressures on the GC-content of prokaryotic and viral genomes. In some bacteria this may reflect needs for thermal stability, but in others it seems to be random drift (see e.g. Biology SE questions on GC-content of genomes).

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Codon usage is not necessarily associated with translation efficiency, as your example would illustrate. Though control of translational efficiency and accuracy is one of the well known reasons for the existence of codon usage there have been other hypotheses that link it with asymmetric mutagenesis rates and overall GC content (See "Why does codon usage bias exist?" Novoa & de Pouplana, 2012).

From the same article:

However, the search for a correlation between tRNA abundance and codon usage has been successful only in some organisms [5, 34]. In several species, including many bacteria and eukaryotes, this search has failed [35, 36], prompting the proposal that, in the latter organisms, translation efficiency might not be the primary factor influencing codon usage [36, 37]. However, it was recently reported that two distinct modifications at the wobble position of certain anticodons are at the core of this apparent lack of correlation [28].

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