> This is surprising because individual tRNA abundance varies by cell state and type, so that would have been the obvious (but apparently wrong) explanation. t

> This is surprising because individual tRNA abundance varies by cell state and type, so that would have been the obvious (but apparently wrong) explanation. tRNA gene expression varies by cell state, but isoacceptor abundance is in fact very stable (at least in mammals). Meaning, if you have a set of tRNA genes which all code for, say, Ala_AGC, the sum of the gene expression of all these genes is relatively stable, even if their individual expression varies (http://dx.doi.org/10.1101/gr.176784.114l; http://dx.doi.org/10.1101/gr.176784.114l; full disclosure: I’m an author on this and one of the previously linked papers). Why individual tRNA gene expression varies, and how the cell regulates the overall stability, is unclear (my personal pet theory is that secondary tRNA function as regulatory RNA, in the form of tRNA-derived fragments, causes the need to regulate tRNA genes, see e.g. http://dx.doi.org/10.1016/j.cell.2017.06.013 http://dx.doi.org/10.1016/j.cell.2017.06.013). > It's doubly surprising because a number of single celled organisms utilize the mismatch between codon preference and tRNA availability in order to regulate protein translation It’s not that surprising: gene regulation happens fundamentally differently in eukaryotes and prokaryotes, and even differently in different classes of eukaryotes. The effective population size (= evolvability) and genome complexity seems to play a role here. Simply put, higher animals have much more powerful and precise ways of controlling gene expression (enhancers and histone control). Regulation at the translation level is comparatively slow and wasteful (it’s several steps further down the line of the gene->protein production process).