Örd Mihkel, Winters Matthew J, Subbanna Mythili S, Garrido Natalia de Martin, Cushing Victoria I, Kliche Johanna, Benz Caroline, Ivarsson Ylva, Greber Basil J, Pryciak Peter M, Davey Norman E
University of Cambridge, CRUK Cambridge Institute, Cambridge, UK.
The Institute of Cancer Research, Chester Beatty Laboratories, 237 Fulham Road, London, SW3 6JB, UK.
bioRxiv. 2024 Dec 4:2024.12.03.625240. doi: 10.1101/2024.12.03.625240.
Cyclin-CDKs are master regulators of cell division. In addition to directly activating the CDK, the cyclin subunit regulates CDK specificity by binding short peptide "docking" motifs in CDK substrates. Here, we measure the relative binding strength of ~100,000 peptides to 11 human cyclins from five cyclin families (D, E, A, B and F). Using a quantitative intracellular binding assay and large-scale tiled peptide screening, we identified a range of non-canonical binders that unveil a broader than anticipated repertoire of cyclin docking motif types. Structural and saturation mutagenesis studies revealed distinct binding modes and sequence features that govern motif recognition, binding strength, and cyclin preference. Docking motifs vary from highly selective to pan-cyclin, thereby fine-tuning the timing of CDK phosphorylation during cell cycle progression. Overall, these findings provide an unprecedented depth of understanding about the rules encoding specificity and affinity within a group of related but distinct protein domains.
细胞周期蛋白依赖性激酶(Cyclin-CDKs)是细胞分裂的主要调节因子。除了直接激活CDK外,细胞周期蛋白亚基还通过结合CDK底物中的短肽“对接”基序来调节CDK的特异性。在这里,我们测量了约100,000种肽与来自五个细胞周期蛋白家族(D、E、A、B和F)的11种人类细胞周期蛋白的相对结合强度。使用定量细胞内结合测定法和大规模平铺肽筛选,我们鉴定出一系列非典型结合物,这些结合物揭示了比预期更广泛的细胞周期蛋白对接基序类型。结构和饱和诱变研究揭示了控制基序识别、结合强度和细胞周期蛋白偏好的不同结合模式和序列特征。对接基序从高度选择性到泛细胞周期蛋白各不相同,从而在细胞周期进程中微调CDK磷酸化的时间。总体而言,这些发现为理解一组相关但不同的蛋白质结构域内编码特异性和亲和力的规则提供了前所未有的深度。