Galmozzi Carla Verónica, Tippmann Frank, Wruck Florian, Auburger Josef Johannes, Kats Ilia, Guennigmann Manuel, Till Katharina, O Brien Edward P, Tans Sander J, Kramer Günter, Bukau Bernd
Center for Molecular Biology of Heidelberg University (ZMBH), DKFZ-ZMBH Alliance, Heidelberg, Germany.
Instituto de Biomedicina de Sevilla, Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, Seville, Spain.
Nat Commun. 2025 May 10;16(1):4361. doi: 10.1038/s41467-025-59067-9.
Chaperones are essential to the co-translational folding of most proteins. However, the principles of co-translational chaperone interaction throughout the proteome are poorly understood, as current methods are restricted to few substrates and cannot capture nascent protein folding or chaperone binding sites, precluding a comprehensive understanding of productive and erroneous protein biosynthesis. Here, by integrating genome-wide selective ribosome profiling, single-molecule tools, and computational predictions using AlphaFold we show that the binding of the main E. coli chaperones involved in co-translational folding, Trigger Factor (TF) and DnaK correlates with "unsatisfied residues" exposed on nascent partial folds - residues that have begun to form tertiary structure but cannot yet form all native contacts due to ongoing translation. This general principle allows us to predict their co-translational binding across the proteome based on sequence only, which we verify experimentally. The results show that TF and DnaK stably bind partially folded rather than unfolded conformers. They also indicate a synergistic action of TF guiding intra-domain folding and DnaK preventing premature inter-domain contacts, and reveal robustness in the larger chaperone network (TF, DnaK, GroEL). Given the complexity of translation, folding, and chaperone functions, our predictions based on general chaperone binding rules indicate an unexpected underlying simplicity.
分子伴侣对于大多数蛋白质的共翻译折叠至关重要。然而,由于目前的方法仅限于少数底物,无法捕捉新生蛋白质的折叠或分子伴侣结合位点,因此人们对整个蛋白质组中共翻译分子伴侣相互作用的原理了解甚少,这使得我们无法全面理解蛋白质生物合成的有效过程和错误过程。在这里,通过整合全基因组选择性核糖体分析、单分子工具以及使用AlphaFold进行的计算预测,我们发现参与共翻译折叠的主要大肠杆菌分子伴侣触发因子(TF)和DnaK的结合与新生部分折叠中暴露的“未满足残基”相关——这些残基已开始形成三级结构,但由于正在进行的翻译而尚未形成所有天然接触。这一普遍原理使我们仅基于序列就能预测它们在整个蛋白质组中的共翻译结合情况,我们通过实验验证了这一点。结果表明,TF和DnaK稳定地结合部分折叠而非未折叠的构象。它们还表明了TF引导结构域内折叠和DnaK防止结构域间过早接触的协同作用,并揭示了更大的分子伴侣网络(TF、DnaK、GroEL)的稳健性。鉴于翻译、折叠和分子伴侣功能的复杂性,我们基于一般分子伴侣结合规则的预测表明存在意想不到的潜在简单性。