From the ‡Stowers Institute for Medical Research, Kansas City, MO 64110.
From the ‡Stowers Institute for Medical Research, Kansas City, MO 64110;
Mol Cell Proteomics. 2018 Jul;17(7):1432-1447. doi: 10.1074/mcp.TIR118.000661. Epub 2018 Mar 29.
Although a variety of affinity purification mass spectrometry (AP-MS) strategies have been used to investigate complex interactions, many of these are susceptible to artifacts because of substantial overexpression of the exogenously expressed bait protein. Here we present a logical and systematic workflow that uses the multifunctional Halo tag to assess the correct localization and behavior of tagged subunits of the Sin3 histone deacetylase complex prior to further AP-MS analysis. Using this workflow, we modified our tagging/expression strategy with 21.7% of the tagged bait proteins that we constructed, allowing us to quickly develop validated reagents. Specifically, we apply the workflow to map interactions between stably expressed versions of the Sin3 subunits SUDS3, SAP30, or SAP30L and other cellular proteins. Here we show that the SAP30 and SAP30L paralogues strongly associate with the core Sin3 complex, but SAP30L has unique associations with the proteasome and the myelin sheath. Next, we demonstrate an advancement of the complex NSAF (cNSAF) approach, in which normalization to the scaffold protein SIN3A accounts for variations in the proportion of each bait capturing Sin3 complexes and allows a comparison among different baits capturing the same protein complex. This analysis reveals that although the Sin3 subunit SUDS3 appears to be used in both SIN3A and SIN3B based complexes, the SAP30 subunit is not used in SIN3B based complexes. Intriguingly, we do not detect the Sin3 subunits SAP18 and SAP25 among the 128 high-confidence interactions identified, suggesting that these subunits may not be common to all versions of the Sin3 complex in human cells. This workflow provides the framework for building validated reagents to assemble quantitative interaction networks for chromatin remodeling complexes and provides novel insights into focused protein interaction networks.
尽管已经使用了多种亲和纯化质谱 (AP-MS) 策略来研究复杂的相互作用,但由于外源表达的诱饵蛋白的大量过表达,许多这些策略都容易受到人为干扰。在这里,我们提出了一种逻辑和系统的工作流程,该流程使用多功能 Halo 标签来评估 Sin3 组蛋白去乙酰化酶复合物标记亚基的正确定位和行为,然后再进行进一步的 AP-MS 分析。使用此工作流程,我们修改了我们的标记/表达策略,使我们构建的 21.7%的标记诱饵蛋白能够快速开发经过验证的试剂。具体来说,我们将该工作流程应用于稳定表达的 Sin3 亚基 SUDS3、SAP30 或 SAP30L 及其它细胞蛋白之间相互作用的映射。在这里,我们表明 SAP30 和 SAP30L 同源物与核心 Sin3 复合物强烈相关,但 SAP30L 与蛋白酶体和髓鞘具有独特的关联。接下来,我们展示了复杂非特异性吸附因子 (cNSAF) 方法的改进,该方法通过将归一化到支架蛋白 SIN3A 来校正每个诱饵捕获 Sin3 复合物的比例变化,从而允许在不同的诱饵之间进行比较,这些诱饵捕获相同的蛋白复合物。这种分析表明,尽管 Sin3 亚基 SUDS3 似乎存在于基于 SIN3A 和 SIN3B 的复合物中,但 SAP30 亚基不存在于基于 SIN3B 的复合物中。有趣的是,我们在鉴定的 128 个高可信度相互作用中没有检测到 Sin3 亚基 SAP18 和 SAP25,这表明这些亚基可能不是人类细胞中所有版本的 Sin3 复合物的常见亚基。该工作流程为构建经过验证的试剂提供了框架,用于组装染色质重塑复合物的定量相互作用网络,并为聚焦蛋白相互作用网络提供了新的见解。