Gardner Timothy S, di Bernardo Diego, Lorenz David, Collins James J
Center for BioDynamics and Department of Biomedical Engineering, Boston University, 44 Cummington Street, Boston, MA 02215, USA.
Science. 2003 Jul 4;301(5629):102-5. doi: 10.1126/science.1081900.
The complexity of cellular gene, protein, and metabolite networks can hinder attempts to elucidate their structure and function. To address this problem, we used systematic transcriptional perturbations to construct a first-order model of regulatory interactions in a nine-gene subnetwork of the SOS pathway in Escherichia coli. The model correctly identified the major regulatory genes and the transcriptional targets of mitomycin C activity in the subnetwork. This approach, which is experimentally and computationally scalable, provides a framework for elucidating the functional properties of genetic networks and identifying molecular targets of pharmacological compounds.
细胞基因、蛋白质和代谢物网络的复杂性可能会阻碍阐明其结构和功能的尝试。为了解决这个问题，我们使用系统的转录扰动来构建大肠杆菌SOS途径九基因子网络中调控相互作用的一阶模型。该模型正确识别了子网络中的主要调控基因和丝裂霉素C活性的转录靶点。这种方法在实验和计算上具有可扩展性，为阐明遗传网络的功能特性和识别药理化合物的分子靶点提供了一个框架。
