Institute for Bioscience and Biotechnology Research, University of Maryland, Rockville, Maryland, United States of America.
PLoS One. 2012;7(7):e41912. doi: 10.1371/journal.pone.0041912. Epub 2012 Jul 25.
Human RON (Recepteur d'Origine Nantais) receptor tyrosine kinase is a cell surface receptor for Macrophage Stimulating Protein (MSP). RON mediates signal transduction pathways that regulate cell adhesion, invasion, motility and apoptosis processes. Elevated levels of RON and its alternatively spliced variants are implicated in the progression and metastasis of tumor cells. The binding of MSP α/β heterodimer to the extracellular region of RON receptor induces receptor dimerization and activation by autophosphorylation of the intracellular kinase domains. The ectodomain of RON, containing the ligand recognition and dimerization domains, is composed of a semaphorin (Sema), Plexins-Semaphorins-Integrins domain (PSI), and four Immunoglobulins-Plexins-Transcription factor (IPT) domains. High affinity association between MSP and RON is mediated by the interaction between MSP β-chain and RON Sema, although RON activation requires intact RON and MSP proteins. Here, we report the structure of RON Sema-PSI domains at 1.85 Å resolution. RON Sema domain adopts a seven-bladed β-propeller fold, followed by disulfide bond rich, cysteine-knot PSI motif. Comparison with the homologous Met receptor tyrosine kinase reveals that RON Sema-PSI contains distinguishing secondary structural features. These define the receptors' exclusive selectivity towards their respective ligands, RON for MSP and Met for HGF. The RON Sema-PSI crystal packing generates a homodimer with interface formed by the Sema domain. Mapping of the dimer interface using the RON homology to Met, MSP homology to Hepatocyte Growth Factor (HGF), and the structure of the Met/HGF complex shows the dimer interface overlapping with the putative MSPβ binding site. The crystallographically determined RON Sema-PSI homodimer may represent the dimer assembly that occurs during ligand-independent receptor activation and/or the inhibition of the constitutive activity of RONΔ160 splice variant by the soluble RON splice variant, RONΔ85.
人RON(Nantais 来源受体)受体酪氨酸激酶是巨噬细胞刺激蛋白(MSP)的细胞表面受体。RON 介导信号转导途径,调节细胞黏附、侵袭、运动和凋亡过程。RON 及其选择性剪接变体的水平升高与肿瘤细胞的进展和转移有关。MSPα/β 异二聚体与 RON 受体的细胞外区结合,诱导受体二聚化,并通过细胞内激酶结构域的自身磷酸化激活。RON 的胞外结构域,包含配体识别和二聚化结构域,由一个 semaphorin(Sema)、Plexins-Semaphorins-Integrins 结构域(PSI)和四个 Immunoglobulins-Plexins-Transcription factor(IPT)结构域组成。MSP 和 RON 之间的高亲和力结合是通过 MSPβ 链与 RON Sema 之间的相互作用介导的,尽管 RON 激活需要完整的 RON 和 MSP 蛋白。在这里,我们报道了 RON Sema-PSI 结构域在 1.85 Å分辨率下的结构。RON Sema 结构域采用七叶桨β-螺旋折叠,随后是富含二硫键的半胱氨酸结 PSI 基序。与同源的 Met 受体酪氨酸激酶的比较表明,RON Sema-PSI 包含独特的二级结构特征。这些特征定义了受体对各自配体的独特选择性,RON 对 MSP,Met 对 HGF。RON Sema-PSI 晶体包装生成同源二聚体,界面由 Sema 结构域形成。使用 RON 同源物到 Met、MSP 同源物到 Hepatocyte Growth Factor(HGF)和 Met/HGF 复合物的结构对二聚体界面进行映射表明,二聚体界面与假定的 MSPβ 结合位点重叠。通过晶体学确定的 RON Sema-PSI 同源二聚体可能代表配体非依赖性受体激活期间发生的二聚体组装和/或可溶性 RON 剪接变体对 RONΔ160 剪接变体组成型活性的抑制。