Deficiency of the ribosomal protein uS10 (RPS20) reorganizes human cells translatome according to the abundance, CDS length and GC content of mRNAs.

IF 4.5 3区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Open Biology Pub Date : 2024-01-01 Epub Date: 2024-01-31 DOI:10.1098/rsob.230366
Yueming Tian, Elena S Babaylova, Alexander V Gopanenko, Alexey E Tupikin, Marsel R Kabilov, Alexey A Malygin
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引用次数: 0

Abstract

Ribosomal protein uS10, a product of the RPS20 gene, is an essential constituent of the small (40S) subunit of the human ribosome. Disruptive mutations in its gene are associated with a predisposition to hereditary colorectal carcinoma. Here, using HEK293T cells, we show that a deficiency of this protein leads to a decrease in the level of ribosomes (ribosomal shortage). RNA sequencing of the total and polysome-associated mRNA samples reveals hundreds of genes differentially expressed in the transcriptome (t)DEGs and translatome (p)DEGs under conditions of uS10 deficiency. We demonstrate that the (t)DEG and (p)DEG sets partially overlap, determine genes with altered translational efficiency (TE) and identify cellular processes affected by uS10 deficiency-induced ribosomal shortage. We reveal that translated mRNAs of upregulated (p)DEGs and genes with altered TE in uS10-deficient cells are generally more abundant and that their GC contents are significantly lower than those of the respective downregulated sets. We also observed that upregulated (p)DEGs have longer coding sequences. Based on our findings, we propose a combinatorial model describing the process of reorganization of mRNA translation under conditions of ribosomal shortage. Our results reveal rules according to which ribosomal shortage reorganizes the transcriptome and translatome repertoires of actively proliferating cells.

核糖体蛋白uS10(RPS20)的缺乏会根据mRNA的丰度、CDS长度和GC含量重组人体细胞的翻译组。
核糖体蛋白 uS10 是 RPS20 基因的产物,是人类核糖体小亚基(40S)的重要组成部分。其基因的破坏性突变与遗传性结直肠癌的易感性有关。在这里,我们利用 HEK293T 细胞证明,缺乏这种蛋白质会导致核糖体水平下降(核糖体缺乏)。总mRNA和多聚体相关mRNA样本的RNA测序显示,在uS10缺乏的条件下,数百个基因在转录组(t)DEG和转译组(p)DEG中差异表达。我们证明(t)DEG和(p)DEG集部分重叠,确定了翻译效率(TE)改变的基因,并确定了受uS10缺乏引起的核糖体短缺影响的细胞过程。我们发现,在uS10缺乏的细胞中,上调(p)DEG和TE改变的基因的翻译mRNA通常更丰富,其GC含量明显低于相应的下调集。我们还观察到,上调(p)DEGs 的编码序列较长。根据我们的研究结果,我们提出了一个组合模型,描述了核糖体短缺条件下 mRNA 翻译的重组过程。我们的研究结果揭示了核糖体短缺重组活跃增殖细胞转录组和翻译组的规则。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Open Biology
Open Biology BIOCHEMISTRY & MOLECULAR BIOLOGY-
CiteScore
10.00
自引率
1.70%
发文量
136
审稿时长
6-12 weeks
期刊介绍: Open Biology is an online journal that welcomes original, high impact research in cell and developmental biology, molecular and structural biology, biochemistry, neuroscience, immunology, microbiology and genetics.
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