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首页> 外文期刊>Journal of Molecular Biology >Protein synthesis factors (RF1, RF2, RF3, RRF, and tmRNA) and peptidyl-tRNA hydrolase rescue stalled ribosomes at sense codons
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Protein synthesis factors (RF1, RF2, RF3, RRF, and tmRNA) and peptidyl-tRNA hydrolase rescue stalled ribosomes at sense codons

机译：蛋白质合成因子（RF1，RF2，RF3，RRF和tmRNA）和肽基-tRNA水解酶以有义密码子拯救失速的核糖体

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During translation, ribosomes stall on mRNA when the aminoacyl-tRNA to be read is not readily available. The stalled ribosomes are deleterious to the cell and should be rescued to maintain its viability. To investigate the contribution of some of the cellular translation factors on ribosome rescuing, we provoked stalling at AGA codons in mutants that affected the factors and then analyzed the accumulation of oligopeptidyl (peptides of up to 6 amino acid residues, oligopep-)-tRNA or polypeptidyl (peptides of more than 300 amino acids in length, polypep-)-tRNA associated with ribosomes. Stalling was achieved by starvation for aminoacyl-tRNA Arg4 upon induced expression of engineered lacZ (β-galactosidase) reporter gene harboring contiguous AGA codons close to the initiation codon or at internal codon positions together with minigene ATGAGATAA accompanied by reduced peptidyl-tRNA hydrolase (Pth). Our results showed accumulations of peptidyl-tRNA associated with ribosomes in mutants for release factors (RF1, RF2, and RF3), ribosome recycling factor (RRF), Pth, and transfer-messenger RNA (tmRNA), implying that each of these factors cooperate in rescuing stalled ribosomes. The role of these factors in ribosome releasing from the stalled complex may vary depending on the length of the peptide in the peptidyl-tRNA. RF3 and RRF rescue stalled ribosomes by "drop-off" of peptidyl-tRNA, while RF1, RF2 (in the absence of termination codon), or Pth may rescue by hydrolyzing the associated peptidyl-tRNA. This is followed by the disassembly of the ribosomal complex of tRNA and mRNA by RRF and elongation factor G.
机译：在翻译过程中，当待读取的氨酰-tRNA不易获得时，核糖体停在mRNA上。停滞的核糖体对细胞有害，应予以挽救以维持其生存能力。为了研究某些细胞翻译因子对核糖体拯救的贡献，我们在影响该因子的突变体中引起了AGA密码子的失速，然后分析了寡肽（最多6个氨基酸残基的肽，寡聚-）-tRNA或与核糖体相关的多肽基肽（长度超过300个氨基酸的多肽，polypep-）-tRNA。失速是通过诱导工程化lacZ（β-半乳糖苷酶）报告基因基因表达饥饿而实现的，该基因带有接近起始密码子或内部密码子位置的连续AGA密码子，与小基因ATGAGATAA伴随着减少的肽基-tRNA水解酶（Pth ）。我们的研究结果表明，与核糖体相关的肽基-tRNA在突变体中具有释放因子（RF1，RF2和RF3），核糖体回收因子（RRF），Pth和转移信使RNA（tmRNA）的突变，这意味着这些因子中的每一个都可以协同作用营救失速的核糖体。这些因素在核糖体从失速复合物中释放的作用可能根据肽基-tRNA中肽段的长度而变化。 RF3和RRF通过“脱除”肽基tRNA来拯救失速的核糖体，而RF1，RF2（在没有终止密码子的情况下）或Pth可以通过水解相关的肽基tRNA来拯救。随后是RRF和延伸因子G分解tRNA和mRNA的核糖体复合物。

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