Begley Thomas J, Rosenbach Ari S, Ideker Trey, Samson Leona D
Biological Engineering Division and Center for Environmental Health Sciences, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA.
Mol Cell. 2004 Oct 8;16(1):117-25. doi: 10.1016/j.molcel.2004.09.005.
DNA repair and checkpoint pathways protect against carcinogen-induced toxicity. Here, we describe additional, equally protective pathways discovered by interrogating 4,733 yeast proteins for their ability to diminish toxicity induced by four known carcinogens. A computational mapping strategy for global phenotypic data was developed to build a systems toxicology model detailing recovery from carcinogen exposure and identifying protein complexes that modulate toxicity. Global phenotypic data were merged with global subcellular localization and protein interactome data to generate an integrated picture of cellular recovery after carcinogen exposure. Statistically validated results from this systems-wide integration demonstrate that, in addition to the nucleus, subnetworks of toxicity-modulating proteins were overrepresented in the vacuolar membrane, endosome, endoplasmic reticulum, and mitochondrion. In addition, we show that many proteins associated with RNA polymerase II, macromolecular trafficking, and vacuole function can now be counted among the many proteins that modulate carcinogen-induced toxicity.
DNA修复和检查点通路可抵御致癌物诱导的毒性。在此,我们描述了通过检测4733种酵母蛋白降低四种已知致癌物诱导毒性的能力而发现的其他同样具有保护作用的通路。我们开发了一种针对全局表型数据的计算映射策略,以构建一个系统毒理学模型,详细说明致癌物暴露后的恢复情况,并识别调节毒性的蛋白质复合物。将全局表型数据与全局亚细胞定位和蛋白质相互作用组数据合并,以生成致癌物暴露后细胞恢复的综合图景。这种全系统整合的经统计学验证的结果表明,除细胞核外,毒性调节蛋白的子网络在液泡膜、内体、内质网和线粒体中也有过度表达。此外,我们表明,现在许多与RNA聚合酶II、大分子运输和液泡功能相关的蛋白质也可被视为调节致癌物诱导毒性的众多蛋白质之一。