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真核核糖体特有的 uL11 的柔性 N 端基序与 P 复合物相互作用,促进蛋白质翻译。

The flexible N-terminal motif of uL11 unique to eukaryotic ribosomes interacts with P-complex and facilitates protein translation.

机构信息

School of Life Sciences, Centre for Protein Science and Crystallography, State Key Laboratory of Agrobiotechnology, The Chinese University of Hong Kong, Shatin, Hong Kong, China.

Department of Biology, Faculty of Science, Niigata University, Ikarashi 2-8050, Nishi-ku, Niigata 950-2181, Japan.

出版信息

Nucleic Acids Res. 2022 May 20;50(9):5335-5348. doi: 10.1093/nar/gkac292.

Abstract

Eukaryotic uL11 contains a conserved MPPKFDP motif at the N-terminus that is not found in archaeal and bacterial homologs. Here, we determined the solution structure of human uL11 by NMR spectroscopy and characterized its backbone dynamics by 15N-1H relaxation experiments. We showed that these N-terminal residues are unstructured and flexible. Structural comparison with ribosome-bound uL11 suggests that the linker region between the N-terminal domain and C-terminal domain of human uL11 is intrinsically disordered and only becomes structured when bound to the ribosomes. Mutagenesis studies show that the N-terminal conserved MPPKFDP motif is involved in interacting with the P-complex and its extended protuberant domain of uL10 in vitro. Truncation of the MPPKFDP motif also reduced the poly-phenylalanine synthesis in both hybrid ribosome and yeast mutagenesis studies. In addition, G→A/P substitutions to the conserved GPLG motif of helix-1 reduced poly-phenylalanine synthesis to 9-32% in yeast ribosomes. We propose that the flexible N-terminal residues of uL11, which could extend up to ∼25 Å from the N-terminal domain of uL11, can form transient interactions with the uL10 that help to fetch and fix it into a position ready for recruiting the incoming translation factors and facilitate protein synthesis.

摘要

真核生物 uL11 的 N 端含有一个保守的 MPPKFDP 基序,该基序在古菌和细菌同源物中不存在。在这里,我们通过 NMR 光谱法测定了人 uL11 的溶液结构,并通过 15N-1H 弛豫实验表征了其骨架动力学。我们表明这些 N 端残基没有结构且灵活。与结合核糖体的 uL11 的结构比较表明,人 uL11 的 N 端结构域和 C 端结构域之间的连接区是固有无序的,只有与核糖体结合时才会变得有结构。突变研究表明,N 端保守的 MPPKFDP 基序参与与 P 复合物及其在体外的延伸突出结构域的相互作用。MPPKFDP 基序的截断也减少了杂种核糖体和酵母突变研究中的多苯丙氨酸合成。此外,螺旋 1 中保守的 GPLG 基序的 G→A/P 取代使酵母核糖体中的多苯丙氨酸合成减少到 9-32%。我们提出,uL11 的柔性 N 端残基可以从 uL11 的 N 端结构域延伸长达约 25 Å,可以与 uL10 形成瞬时相互作用,帮助其获取并固定在准备招募传入翻译因子的位置,并促进蛋白质合成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f89/9122527/6bcdc89093d9/gkac292fig1.jpg

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