TC Jenkins Department of Biophysics, Johns Hopkins University, Baltimore, MD 21218, USA.
J Mol Biol. 2011 Nov 25;414(2):243-59. doi: 10.1016/j.jmb.2011.09.050. Epub 2011 Oct 6.
The Notch signal transduction pathway controls cell fate determination during metazoan development. The Notch gene encodes a transmembrane receptor that is cleaved upon activation, liberating the Notch intracellular domain, which enters the nucleus and assembles transcriptional activation complexes that drive expression of Notch-responsive genes. The most conserved region of the Notch intracellular domain is an ankyrin domain (Nank), which binds directly to the cytosolic effector protein Deltex (Dx), controlling intracellular Notch activity. However, the structural and energetic basis for this interaction remains unknown. Here, we analyze the thermodynamics and hydrodynamics of the Nank:Dx heteroassociation, as well as a weaker Nank self-association, using sedimentation velocity analytical ultracentrifugation. By comparing g(s*) and c(s) distributions, and by direct fitting of sedimentation boundaries with thermodynamic association models, we were able to characterize the Nank:Dx heterodimer, measure its affinity, and map the interaction on the surface on Nank. N- and C-terminal deletions of whole ankyrin units implicate repeats 3 and 4 as key for mediating heteroassociation. An alanine scan across the interaction loops of Nank identifies a conserved hot spot in repeats 3 and 4, centered at R127, as critical for Dx binding. In addition, we were able to detect weak but reproducible Nank homodimerization (K(d) in the millimolar range). This association is disrupted by substitution of a conserved arginine (R107) with alanine, a residue previously implicated in a functionally relevant mode of interaction within dimeric transcription complexes. The distinct binding surfaces on Nank for homotypic versus Dx interaction appear to be compatible with teterameric Notch(2):Dx(2) assembly.
Notch 信号转导通路在后生动物发育过程中控制细胞命运的决定。Notch 基因编码一种跨膜受体,该受体在激活时被切割,释放 Notch 细胞内结构域,该结构域进入细胞核并组装转录激活复合物,驱动 Notch 反应基因的表达。Notch 细胞内结构域最保守的区域是锚蛋白重复结构域(Nank),它直接与细胞质效应蛋白 Deltex(Dx)结合,控制细胞内 Notch 活性。然而,这种相互作用的结构和能量基础仍然未知。在这里,我们使用沉降速度分析超速离心法分析 Nank:Dx 异源二聚体以及较弱的 Nank 自组装的热力学和流体动力学。通过比较 g(s*)和 c(s)分布,并通过直接用热力学关联模型拟合沉降边界,我们能够表征 Nank:Dx 异二聚体,测量其亲和力,并在 Nank 表面上绘制相互作用图。整个锚蛋白重复单元的 N 和 C 末端缺失暗示重复 3 和 4 是介导异源二聚体形成的关键。在 Nank 的相互作用环上进行的丙氨酸扫描确定了重复 3 和 4 中的保守热点,以 R127 为中心,对 Dx 结合至关重要。此外,我们能够检测到微弱但可重复的 Nank 同源二聚化(在毫摩尔范围内的 K(d))。这种结合被用丙氨酸取代保守的精氨酸(R107)破坏,该残基先前涉及二聚体转录复合物中功能相关的相互作用模式。Nank 上用于同型与 Dx 相互作用的不同结合表面似乎与四聚体 Notch(2):Dx(2)组装兼容。