核糖体
生物
核糖体分析
真核核糖体
细胞生物学
核糖体蛋白
伴侣(临床)
蛋白质生物合成
翻译(生物学)
信使核糖核酸
生物化学
核糖核酸
基因
医学
病理
作者
Yoon-Mo Yang,Young-Eun Jung,Daniel Abegg,Alexander Adibekian,Kate S. Carroll,Katrin Karbstein
出处
期刊:Molecular Cell
[Elsevier]
日期:2023-05-01
卷期号:83 (9): 1527-1537.e5
被引量:6
标识
DOI:10.1016/j.molcel.2023.03.030
摘要
Because of the central role ribosomes play for protein translation and ribosome-mediated mRNA and protein quality control (RQC), the ribosome pool is surveyed and dysfunctional ribosomes degraded both during assembly, as well as the functional cycle. Oxidative stress downregulates translation and damages mRNAs and ribosomal proteins (RPs). Although damaged mRNAs are detected and degraded via RQC, how cells mitigate damage to RPs is not known. Here, we show that cysteines in Rps26 and Rpl10 are readily oxidized, rendering the proteins non-functional. Oxidized Rps26 and Rpl10 are released from ribosomes by their chaperones, Tsr2 and Sqt1, and the damaged ribosomes are subsequently repaired with newly made proteins. Ablation of this pathway impairs growth, which is exacerbated under oxidative stress. These findings reveal an unanticipated mechanism for chaperone-mediated ribosome repair, augment our understanding of ribosome quality control, and explain previous observations of protein exchange in ribosomes from dendrites, with broad implications for aging and health.
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