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Title: Codon bias confers stability to human mRNAs
Authors: Hia, Fabian
Yang, Sheng Fan
Shichino, Yuichi
Yoshinaga, Masanori  kyouindb  KAKEN_id
Murakawa, Yasuhiro  kyouindb  KAKEN_id  orcid (unconfirmed)
Vandenbon, Alexis  kyouindb  KAKEN_id  orcid (unconfirmed)
Fukao, Akira
Fujiwara, Toshinobu
Landthaler, Markus
Natsume, Tohru
Adachi, Shungo
Iwasaki, Shintaro
Takeuchi, Osamu  kyouindb  KAKEN_id  orcid (unconfirmed)
Author's alias: ヒヤ, フェビエン
ヤン, シェン ファン
七野, 悠一
吉永, 正憲
村川, 泰裕
深尾, 亜喜良
藤原, 俊伸
夏目, 徹
足達, 俊吾
岩崎, 信太郎
竹内, 理
Keywords: codon bias
codon optimality
mRNA stability
transla-tion efficiency
Issue Date: 5-Nov-2019
Publisher: EMBO Press
Journal title: EMBO reports
Volume: 20
Issue: 11
Thesis number: e48220
Abstract: Codon bias has been implicated as one of the major factors contributing to mRNA stability in several model organisms. However, the molecular mechanisms of codon bias on mRNA stability remain unclear in humans. Here, we show that human cells possess a mechanism to modulate RNA stability through a unique codon bias. Bioinformatics analysis showed that codons could be clustered into two distinct groups--codons with G or C at the third base position (GC3) and codons with either A or T at the third base position (AT3): the former stabilizing while the latter destabilizing mRNA. Quantification of codon bias showed that increased GC3‐content entails proportionately higher GC‐content. Through bioinformatics, ribosome profiling, and in vitro analysis, we show that decoupling the effects of codon bias reveals two modes of mRNA regulation, one GC3‐ and one GC‐content dependent. Employing an immunoprecipitation‐based strategy, we identify ILF2 and ILF3 as RNA‐binding proteins that differentially regulate global mRNA abundances based on codon bias. Our results demonstrate that codon bias is a two‐pronged system that governs mRNA abundance.
Description: ヒト細胞のコドン(遺伝暗号)に隠された暗号を解明 --ヒトコドン最適化制御による治療戦略の開発へ--. 京都大学プレスリリース. 2019-09-18.
Rights: This is the author’s version of the paper, which has been published in final form at
The full-text file will be made open to the public on 3 March 2020 in accordance with publisher's 'Terms and Conditions for Self-Archiving'.
This is not the published version. Please cite only the published version.
DOI(Published Version): 10.15252/embr.201948220
PubMed ID: 31482640
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