Dey Raja, Ji Kunmei, Liu Zhigang, Chen Lin
Department of Biological Sciences, Molecular and Computational Biology, University of Southern California, Los Angeles, California, United States of America.
PLoS One. 2009;4(4):e5188. doi: 10.1371/journal.pone.0005188. Epub 2009 Apr 7.
Interleukine-3 (IL-3) binds its receptor and initiates a cascade of signaling processes that regulate the proliferation and differentiation of hematopoietic cells. To understand the detailed mechanisms of IL-3 induced receptor activation, we generated a homology model of the IL-3:receptor complex based on the closely related crystal structure of the GM-CSF:receptor complex. Model-predicted interactions between IL-3 and its receptor are in excellent agreement with mutagenesis data, which validate the model and establish a detailed view of IL-3:receptor interaction. The homology structure reveals an IL-3:IL-3 interaction interface in a higher-order complex modeled after the dodecamer of the GM-CSF:receptor complex wherein an analogous GM-CSF:GM-CSF interface is also identified. This interface is mediated by a proline-rich hydrophobic motif (PPLPLL) of the AA' loop that is highly exposed in the structure of isolated IL-3. Various experimental data suggest that this motif is required for IL-3 function through receptor-binding independent mechanisms. These observations are consistent with structure-function studies of the GM-CSF:receptor complex showing that formation of the higher-order cytokine:receptor complex is required for signaling. However, a key question not answered from previous studies is how cytokine binding facilitates the assembly of the higher-order complex. Our studies here reveal a potential cytokine-cytokine interaction that participates in the assembly of the dodecamer complex, thus linking cytokine binding to receptor activation.
白细胞介素-3(IL-3)与其受体结合并启动一系列信号传导过程,这些过程调节造血细胞的增殖和分化。为了了解IL-3诱导受体激活的详细机制,我们基于GM-CSF:受体复合物的紧密相关晶体结构生成了IL-3:受体复合物的同源模型。模型预测的IL-3与其受体之间的相互作用与诱变数据高度吻合,这验证了该模型并建立了IL-3:受体相互作用的详细视图。同源结构揭示了在以GM-CSF:受体复合物的十二聚体为模型的高阶复合物中的IL-3:IL-3相互作用界面,其中也鉴定出了类似的GM-CSF:GM-CSF界面。该界面由AA'环富含脯氨酸的疏水基序(PPLPLL)介导,该基序在分离的IL-3结构中高度暴露。各种实验数据表明,该基序通过不依赖受体结合的机制对IL-3功能是必需的。这些观察结果与GM-CSF:受体复合物的结构-功能研究一致,表明高阶细胞因子:受体复合物的形成是信号传导所必需的。然而,先前研究未回答的一个关键问题是细胞因子结合如何促进高阶复合物的组装。我们这里的研究揭示了一种潜在的细胞因子-细胞因子相互作用,它参与十二聚体复合物的组装,从而将细胞因子结合与受体激活联系起来。