role of reca and the sos response in thymineless death in escherichia colireca和sos反应在大肠杆菌thymineless死亡.pdfVIP

Role of RecA and the SOS Response in Thymineless Death in Escherichia coli 1,2 1,2,3 1 4 1,2,3,5,6 Natalie C. Fonville , David Bates , P. J. Hastings , Philip C. Hanawalt , Susan M. Rosenberg * 1 Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, United States of America, 2 Interdepartmental Graduate Program in Cellular and Molecular Biology, Baylor College of Medicine, Houston, Texas, United States of America, 3 Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas, United States of America, 4 Department of Biological Sciences, Stanford University, Stanford, California, United States of America, 5 Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, Texas, United States of America, 6 Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas, United States of America Abstract Thymineless death (TLD) is a classic and enigmatic phenomenon, documented in bacterial, yeast, and human cells, whereby cells lose viability rapidly when deprived of thymine. Despite its being the essential mode of action of important chemotherapeutic agents, and despite having been studied extensively for decades, the basic mechanisms of TLD have remained elusive. In Escherichia coli, several proteins involved in homologous recombination (HR) are required for TLD, however, surprisingly, RecA, the central HR protein and activator of the SOS DNA–damage response was reported not to be. We demonstrate that RecA and the SOS response are required for a substantial fraction of TLD. We show that some of the Rec proteins implicated previously promote TLD via facili