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重组、减数分裂表达与人类密码子使用偏好性。

Recombination, meiotic expression and human codon usage.

机构信息

Laboratoire de Biométrie et Biologie Evolutive, Université de Lyon, Université Claude Bernard, Villeurbanne, France.

Laboratory of Biology and Modelling of the Cell, UnivLyon, ENS de Lyon, Univ Claude Bernard, CNRS UMR 5239, INSERM U1210, Laboratoire de Biologie et Modélisation de la Cellule, Lyon, France.

出版信息

Elife. 2017 Aug 15;6:e27344. doi: 10.7554/eLife.27344.

DOI:10.7554/eLife.27344
PMID:28826480
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5576983/
Abstract

Synonymous codon usage (SCU) varies widely among human genes. In particular, genes involved in different functional categories display a distinct codon usage, which was interpreted as evidence that SCU is adaptively constrained to optimize translation efficiency in distinct cellular states. We demonstrate here that SCU is not driven by constraints on tRNA abundance, but by large-scale variation in GC-content, caused by meiotic recombination, via the non-adaptive process of GC-biased gene conversion (gBGC). Expression in meiotic cells is associated with a strong decrease in recombination within genes. Differences in SCU among functional categories reflect differences in levels of meiotic transcription, which is linked to variation in recombination and therefore in gBGC. Overall, the gBGC model explains 70% of the variance in SCU among genes. We argue that the strong heterogeneity of SCU induced by gBGC in mammalian genomes precludes any optimization of the tRNA pool to the demand in codon usage.

摘要

同义密码子使用（SCU）在人类基因中差异很大。特别是，参与不同功能类别的基因显示出明显的密码子使用差异，这被解释为 SCU 受到适应性限制，以优化不同细胞状态下的翻译效率的证据。我们在这里证明，SCU 不是由 tRNA 丰度的限制驱动的，而是由减数分裂重组引起的大规模 GC 含量变化驱动的，这是通过非适应性 GC 偏向性基因转换（gBGC）过程实现的。减数分裂细胞中的表达与基因内重组的强烈减少有关。功能类别之间 SCU 的差异反映了减数分裂转录水平的差异，这与重组的差异有关，因此与 gBGC 有关。总体而言，gBGC 模型解释了基因之间 SCU 差异的 70%。我们认为，gBGC 在哺乳动物基因组中诱导的 SCU 强烈异质性排除了对 tRNA 池根据密码子使用需求进行任何优化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/5576983/fd1bfc1db149/elife-27344-resp-fig1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/5576983/fd1bfc1db149/elife-27344-resp-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/5576983/53514fd8fc98/elife-27344-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/5576983/250db5c2e230/elife-27344-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/5576983/0915a8820048/elife-27344-fig2-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/5576983/b05b5022edc7/elife-27344-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/5576983/65f5e119aa42/elife-27344-fig3-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/5576983/79837104401d/elife-27344-fig3-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/5576983/59e5d6baeb4d/elife-27344-fig3-figsupp3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/5576983/137305064de4/elife-27344-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/5576983/3fa42fc903be/elife-27344-fig4-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/5576983/3b79ef175219/elife-27344-fig4-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/5576983/21e839e431d2/elife-27344-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/5576983/0b4019eade96/elife-27344-fig6.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ae1/5576983/fd1bfc1db149/elife-27344-resp-fig1.jpg

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