National Institutes of Health/National Cancer Institute (NIH/NCI)
R01CA282036
米国
National Institutes of Health/National Institute of General Medical Sciences (NIH/NIGMS)
GM135617-01
米国
Cancer Prevention and Research Institute of Texas (CPRIT)
RP220309
米国
Cancer Prevention and Research Institute of Texas (CPRIT)
RR150074
米国
Cancer Prevention and Research Institute of Texas (CPRIT)
RP170644
米国
Welch Foundation
I-1961
米国
Welch Foundation
I-1897
米国
引用
ジャーナル: Science / 年: 2024 タイトル: Specific tRNAs promote mRNA decay by recruiting the CCR4-NOT complex to translating ribosomes. 著者: Xiaoqiang Zhu / Victor Emmanuel Cruz / He Zhang / Jan P Erzberger / Joshua T Mendell / 要旨: The CCR4-NOT complex is a major regulator of eukaryotic messenger RNA (mRNA) stability. Slow decoding during translation promotes association of CCR4-NOT with ribosomes, accelerating mRNA degradation. ...The CCR4-NOT complex is a major regulator of eukaryotic messenger RNA (mRNA) stability. Slow decoding during translation promotes association of CCR4-NOT with ribosomes, accelerating mRNA degradation. We applied selective ribosome profiling to further investigate the determinants of CCR4-NOT recruitment to ribosomes in mammalian cells. This revealed that specific arginine codons in the P-site are strong signals for ribosomal recruitment of human CNOT3, a CCR4-NOT subunit. Cryo-electron microscopy and transfer RNA (tRNA) mutagenesis demonstrated that the D-arms of select arginine tRNAs interact with CNOT3 and promote its recruitment whereas other tRNA D-arms sterically clash with CNOT3. These effects link codon content to mRNA stability. Thus, in addition to their canonical decoding function, tRNAs directly engage regulatory complexes during translation, a mechanism we term P-site tRNA-mediated mRNA decay.
履歴
登録
2024年6月1日
登録サイト: RCSB / 処理サイト: RCSB
改定 1.0
2024年12月4日
Provider: repository / タイプ: Initial release
Remark 0
THIS ENTRY 9C3I REFLECTS AN ALTERNATIVE MODELING OF THE ORIGINAL DATA IN 8BHF, DETERMINED BY ...THIS ENTRY 9C3I REFLECTS AN ALTERNATIVE MODELING OF THE ORIGINAL DATA IN 8BHF, DETERMINED BY Absmeier, E., Chandrasekaran, V., O'Reilly, F.J., Stowell, J.A.W., Rappsilber, J., Passmore, L.A.