Pol III ChIP-seq of liver cancer cell lines

This dataset has been designed to test whether codons in mRNAs and anticodons in tRNAs vary in order to maximize translation in specific cellular conditions in mammals. Prokaryotes and simple unicellular eukaryotes optimize their translational rates by adjusting the codons in the protein-coding transcriptome to the available pool of anticodons in the tRNA transcriptome. We found no evidence supporting this mechanism in mammals, even when subsets of genes were considered, such as those found in Gene Ontology functional categories or in tissue-specific transcriptional signatures. The simplest explanation accounting for the observed codon distributions in mammals is the variation in GC content of gene categories. GC variation across the mammalian genome is most likely to result from the interplay of genome repair and gene duplication mechanisms, rather than selective pressures caused by codon-driven translational rates. This work is part of experiment series: ChIP-Seq E-MTAB-958 and E-MTAB-2326.