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密码子使用偏好与转录终止机制共同进化,以抑制过早的切割和多聚腺苷酸化。

Codon usage biases co-evolve with transcription termination machinery to suppress premature cleavage and polyadenylation.

机构信息

Department of Physiology, The University of Texas Southwestern Medical Center, Dallas, United States.

State Key Laboratory for Conservation and Utilization of Bio-Resources in Yunnan, Yunnan University, Kunming, China.

出版信息

Elife. 2018 Mar 16;7:e33569. doi: 10.7554/eLife.33569.

DOI:10.7554/eLife.33569
PMID:29547124
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5869017/
Abstract

Codon usage biases are found in all genomes and influence protein expression levels. The codon usage effect on protein expression was thought to be mainly due to its impact on translation. Here, we show that transcription termination is an important driving force for codon usage bias in eukaryotes. Using as a model organism, we demonstrated that introduction of rare codons results in premature transcription termination (PTT) within open reading frames and abolishment of full-length mRNA. PTT is a wide-spread phenomenon in and there is a strong negative correlation between codon usage bias and PTT events. Rare codons lead to the formation of putative poly(A) signals and PTT. A similar role for codon usage bias was also observed in mouse cells. Together, these results suggest that codon usage biases co-evolve with the transcription termination machinery to suppress premature termination of transcription and thus allow for optimal gene expression.

摘要

密码子使用偏好存在于所有基因组中,并影响蛋白质表达水平。密码子使用对蛋白质表达的影响被认为主要是由于它对翻译的影响。在这里,我们表明转录终止是真核生物密码子使用偏性的一个重要驱动力。我们以 作为模式生物,证明了稀有密码子的引入会导致开放阅读框内的转录过早终止(PTT),并导致全长 mRNA 的缺失。PTT 是 中一种广泛存在的现象,密码子使用偏性与 PTT 事件之间存在强烈的负相关关系。稀有密码子导致假定的 poly(A) 信号和 PTT 的形成。在小鼠细胞中也观察到了类似的密码子使用偏性的作用。总之,这些结果表明,密码子使用偏性与转录终止机制共同进化,以抑制转录的过早终止,从而实现最佳的基因表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbf8/5869017/6832712f10c3/elife-33569-fig7-figsupp2.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbf8/5869017/aa8967276533/elife-33569-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbf8/5869017/acccbf0c4283/elife-33569-fig7-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbf8/5869017/6832712f10c3/elife-33569-fig7-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbf8/5869017/9cadebc8908b/elife-33569-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbf8/5869017/b80b49e7c4ef/elife-33569-fig1-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbf8/5869017/acd18445f77f/elife-33569-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbf8/5869017/2a8a387bf5b7/elife-33569-fig2-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbf8/5869017/843c30f86628/elife-33569-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbf8/5869017/d201f21f7b6c/elife-33569-fig3-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbf8/5869017/2f257982283c/elife-33569-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbf8/5869017/ff7867a2f8cc/elife-33569-fig4-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbf8/5869017/9b9151c20d0b/elife-33569-fig5.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbf8/5869017/6832712f10c3/elife-33569-fig7-figsupp2.jpg

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