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核糖体在翻译绕过起始时的重排。

Ribosome rearrangements at the onset of translational bypassing.

机构信息

Structural Biology Unit, CIC bioGUNE, 48160 Derio, Spain.

Department of Physical Biochemistry, Max Planck Institute for Biophysical Chemistry, 37077 Göttingen, Germany.

出版信息

Sci Adv. 2017 Jun 7;3(6):e1700147. doi: 10.1126/sciadv.1700147. eCollection 2017 Jun.

DOI:10.1126/sciadv.1700147
PMID:28630923
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5462505/
Abstract

Bypassing is a recoding event that leads to the translation of two distal open reading frames into a single polypeptide chain. We present the structure of a translating ribosome stalled at the bypassing take-off site of of bacteriophage T4. The nascent peptide in the exit tunnel anchors the P-site peptidyl-tRNA to the ribosome and locks an inactive conformation of the peptidyl transferase center (PTC). The mRNA forms a short dynamic hairpin in the decoding site. The ribosomal subunits adopt a rolling conformation in which the rotation of the small subunit around its long axis causes the opening of the A-site region. Together, PTC conformation and mRNA structure safeguard against premature termination and read-through of the stop codon and reconfigure the ribosome to a state poised for take-off and sliding along the noncoding mRNA gap.

摘要

旁路是一种重编码事件，导致两个远端开放阅读框翻译为单个多肽链。我们展示了一个翻译核糖体在噬菌体 T4 的旁路起飞位点停滞的结构。新生肽在出口隧道中锚定 P 位肽酰-tRNA 到核糖体，并锁定肽基转移酶中心（PTC）的非活性构象。mRNA 在解码位点形成一个短的动态发夹。核糖体亚基采用滚动构象，其中小亚基围绕其长轴的旋转导致 A 位点区域的打开。PTC 构象和 mRNA 结构共同防止终止密码子的过早终止和通读，并使核糖体重新配置为准备起飞和沿非编码 mRNA 缺口滑动的状态。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5e2/5462505/540561696b43/1700147-F4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5e2/5462505/05f45e8c2810/1700147-F1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5e2/5462505/aaff5d9d4ddb/1700147-F2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5e2/5462505/efaec7b718fd/1700147-F3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5e2/5462505/540561696b43/1700147-F4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5e2/5462505/05f45e8c2810/1700147-F1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5e2/5462505/aaff5d9d4ddb/1700147-F2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5e2/5462505/efaec7b718fd/1700147-F3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5e2/5462505/540561696b43/1700147-F4.jpg

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Translation regulation via nascent polypeptide-mediated ribosome stalling.通过新生多肽介导的核糖体停滞进行翻译调控。
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Mechanisms of ribosome stalling by SecM at multiple elongation steps.SecM在多个延伸步骤导致核糖体停滞的机制。
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The ribosome termination complex remodels release factor RF3 and ejects GDP.核糖体终止复合物重塑释放因子RF3并排出GDP。
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Kinetics of programmed and spontaneous ribosome sliding along the mRNA.核糖体沿 mRNA 进行程序性和自发性滑动的动力学。
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