Department of Cellular Biochemistry, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany.
Department of Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany.
Proc Natl Acad Sci U S A. 2020 Feb 25;117(8):4099-4108. doi: 10.1073/pnas.1914401117. Epub 2020 Feb 11.
Mammalian cells present a fingerprint of their proteome to the adaptive immune system through the display of endogenous peptides on MHC-I complexes. MHC-I-bound peptides originate from protein degradation by the proteasome, suggesting that stably folded, long-lived proteins could evade monitoring. Here, we investigate the role in antigen presentation of the ribosome-associated quality control (RQC) pathway for the degradation of nascent polypeptides that are encoded by defective messenger RNAs and undergo stalling at the ribosome during translation. We find that degradation of model proteins by RQC results in efficient MHC-I presentation, independent of their intrinsic folding properties. Quantitative profiling of MHC-I peptides in wild-type and RQC-deficient cells by mass spectrometry showed that RQC substantially contributes to the composition of the immunopeptidome. Our results also identify endogenous substrates of the RQC pathway in human cells and provide insight into common principles causing ribosome stalling under physiological conditions.
哺乳动物细胞通过 MHC-I 复合物上展示内源性肽向适应性免疫系统呈现其蛋白质组的“指纹”。MHC-I 结合的肽来源于蛋白酶体对蛋白质的降解,这表明稳定折叠、寿命长的蛋白质可能逃避监测。在这里,我们研究了核糖体相关质量控制 (RQC) 途径在抗原呈递中的作用,该途径可降解由有缺陷的信使 RNA 编码的新生多肽,并在翻译过程中在核糖体上停滞。我们发现,RQC 对模型蛋白的降解导致 MHC-I 的有效呈递,而与它们的固有折叠特性无关。通过质谱对野生型和 RQC 缺陷型细胞中 MHC-I 肽的定量分析表明,RQC 对免疫肽组的组成有很大贡献。我们的研究结果还鉴定了人细胞中 RQC 途径的内源性底物,并深入了解了在生理条件下导致核糖体停滞的常见原理。