Pol III ChIP-seq of liver cancer cell lines. 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.

本数据集旨在检验哺乳动物体内信使RNA（mRNA）的密码子与转运RNA（tRNA）的反密码子是否会发生变异，以在特定细胞条件下最大化翻译效率。原核生物与简单单细胞真核生物可通过将蛋白质编码转录组中的密码子调整至与tRNA转录组中可用的反密码子库相匹配，以此优化翻译速率。我们未发现任何证据支持哺乳动物存在这一机制，即便在考虑特定基因子集的情况下亦是如此——例如归属基因本体（Gene Ontology）功能分类的基因，或是具有组织特异性转录特征的基因。能够解释哺乳动物中观测到的密码子分布的最简假说，为不同基因类别的GC含量存在变异。哺乳动物基因组内的GC含量变异，更可能源于基因组修复与基因复制机制的相互作用，而非密码子驱动的翻译速率所带来的选择压力。本研究隶属于系列实验：ChIP-Seq实验E-MTAB-958与E-MTAB-2326。