Department of Structural Biology, St. Jude Children's Research Hospital, Memphis, TN 38105.
Department of Molecular Machines and Signaling, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany.
Proc Natl Acad Sci U S A. 2019 Aug 27;116(35):17280-17289. doi: 10.1073/pnas.1902889116. Epub 2019 Jul 26.
Ubiquitin (Ub)-mediated proteolysis is a fundamental mechanism used by eukaryotic cells to maintain homeostasis and protein quality, and to control timing in biological processes. Two essential aspects of Ub regulation are conjugation through E1-E2-E3 enzymatic cascades and recognition by Ub-binding domains. An emerging theme in the Ub field is that these 2 properties are often amalgamated in conjugation enzymes. In addition to covalent thioester linkage to Ub's C terminus for Ub transfer reactions, conjugation enzymes often bind noncovalently and weakly to Ub at "exosites." However, identification of such sites is typically empirical and particularly challenging in large molecular machines. Here, studying the 1.2-MDa E3 ligase anaphase-promoting complex/cyclosome (APC/C), which controls cell division and many aspects of neurobiology, we discover a method for identifying unexpected Ub-binding sites. Using a panel of Ub variants (UbVs), we identify a protein-based inhibitor that blocks Ub ligation to APC/C substrates in vitro and ex vivo. Biochemistry, NMR, and cryo-electron microscopy (cryo-EM) structurally define the UbV interaction, explain its inhibitory activity through binding the surface on the APC2 subunit that recruits the E2 enzyme UBE2C, and ultimately reveal that this APC2 surface is also a Ub-binding exosite with preference for K48-linked chains. The results provide a tool for probing APC/C activity, have implications for the coordination of K48-linked Ub chain binding by APC/C with the multistep process of substrate polyubiquitylation, and demonstrate the power of UbV technology for identifying cryptic Ub-binding sites within large multiprotein complexes.
泛素(Ub)介导的蛋白水解是真核细胞维持内稳态和蛋白质质量以及控制生物过程时间的基本机制。Ub 调节的两个重要方面是通过 E1-E2-E3 酶级联反应进行缀合以及通过 Ub 结合结构域进行识别。Ub 领域的一个新兴主题是,这两个特性通常在缀合酶中融合在一起。除了共价硫酯键与 Ub 的 C 末端连接以进行 Ub 转移反应外,缀合酶通常还以“外位”非共价且弱地结合 Ub。然而,此类位点的鉴定通常是经验性的,在大型分子机器中尤其具有挑战性。在这里,我们研究了控制细胞分裂和神经生物学许多方面的 1.2MDa E3 连接酶有丝分裂促进复合物/环体(APC/C),发现了一种识别意外 Ub 结合位点的方法。使用一系列 Ub 变体(UbV),我们鉴定出一种基于蛋白质的抑制剂,该抑制剂可在体外和体内阻止 Ub 连接到 APC/C 底物。生物化学、NMR 和冷冻电镜(cryo-EM)结构定义了 UbV 相互作用,通过结合招募 E2 酶 UBE2C 的 APC2 亚基表面来解释其抑制活性,最终揭示该 APC2 表面也是一个 Ub 结合外位,对 K48 连接链具有偏好性。结果提供了一种探测 APC/C 活性的工具,对 APC/C 与底物多泛素化的多步骤过程中 K48 连接 Ub 链结合的协调具有影响,并证明了 UbV 技术用于在大型多蛋白复合物中识别隐蔽 Ub 结合位点的强大功能。