Orand Thibault, Delaforge Elise, Lee Alexandra, Kragelj Jaka, Tengo Maud, Tengo Laura, Blackledge Martin, Boeri Erba Elisabetta, Davis Roger J, Palencia Andrés, Jensen Malene Ringkjøbing
Université Grenoble Alpes, Commissariat à l'Énergie Atomique et aux Énergies Alternatives, CNRS, Institut de Biologie Structurale, Grenoble 38044, France.
Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01655.
Proc Natl Acad Sci U S A. 2025 Mar 4;122(9):e2419915122. doi: 10.1073/pnas.2419915122. Epub 2025 Feb 25.
Scaffold proteins are key players in many signaling pathways where they ensure spatial and temporal control of molecular interactions by simultaneous tethering of multiple signaling components. The protein JIP1 acts as a scaffold within the c-Jun N-terminal kinase (JNK) signaling pathway by assembling three kinases, MLK3, MKK7, and JNK, into a macromolecular complex that enables their specific activation. The recruitment of these kinases depends on the 450-amino acid intrinsically disordered tail of JIP1, however, the structural details of this tail and the molecular mechanisms by which it binds kinases have remained elusive. Here, we provide an atomic resolution structural description of the JIP1 tail, and we study its interaction with the kinase JNK1. Using NMR spectroscopy, we show that JNK1 not only engages with the well-known docking site motif (D-motif) of JIP1, but also interacts with a noncanonical F-motif. We determine the crystal structure of the JIP1-JNK1 complex at 2.35 Å resolution revealing a bipartite binding mode of JIP1. Our work provides insights into the sequence determinants of F-motifs suggesting that these motifs may be more prevalent in JNK substrates than previously recognized. More broadly, our study highlights the power of NMR spectroscopy in uncovering kinase interaction motifs within disordered scaffold proteins, and it paves the way for atomic-resolution interaction studies of JIP1 with its multitude of interaction partners.
支架蛋白是许多信号通路中的关键参与者,它们通过同时连接多个信号成分来确保分子相互作用的空间和时间控制。蛋白质JIP1在c-Jun氨基末端激酶(JNK)信号通路中作为支架发挥作用,它将三种激酶MLK3、MKK7和JNK组装成一个大分子复合物,使其能够特异性激活。这些激酶的募集取决于JIP1的450个氨基酸的内在无序尾部,然而,该尾部的结构细节及其结合激酶的分子机制仍然难以捉摸。在这里,我们提供了JIP1尾部的原子分辨率结构描述,并研究了它与激酶JNK1的相互作用。使用核磁共振光谱,我们表明JNK1不仅与JIP1的著名对接位点基序(D-基序)结合,还与一个非经典的F-基序相互作用。我们以2.35 Å的分辨率确定了JIP1-JNK1复合物的晶体结构,揭示了JIP1的二分结合模式。我们的工作为F-基序的序列决定因素提供了见解,表明这些基序在JNK底物中可能比以前认识到的更普遍。更广泛地说,我们的研究突出了核磁共振光谱在揭示无序支架蛋白内激酶相互作用基序方面的作用,并为JIP1与其众多相互作用伙伴的原子分辨率相互作用研究铺平了道路。