Role of the SOS Response in Stationary-Phase Hypermutation: A Model for Mutation in Oncogenesis and Chemotherapeutic Drug-Resistance
Abstract
The SOS response of Escherichia coli is the prototypic DNA damage repair and cell cycle control system, analogous to checkpoint control in eukaryotes. The SOS response includes blocking the cell cycle, global mutagenesis via more than one mechanism, and up regulation of DNA repair and recombination functions. Adaptive mutation is a mutational program in non-growing cells subjected to starvation and so is also a temporary mutagenic response to environmental stress. It entails global hypermutation, and previously, the signal transduction pathway from the environment to the DNA was unknown. previously, we demonstrated that adaptive mutation of a lac allele in E. coli is under control of the SOS response, and that SOS induced levels of component(s) other than or in addition to RecA (hRad5l homologue) are also involved. We have demonstrated that the SOS inducible error-prone polymerase DinB/DNA pol TV is required for most adaptive mutation. DNA pol IV is not required for growth-dependent mutation (indicating that it is specific to adaptive mutation) and is not required for repair of RV or oxidative damage lesions. All this is consistent with a role for DNA pol IV for promotion of mutation in response to stress
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 2001
- Accession Number
- ADA396411
Entities
People
- Gregory Mckenzie
Organizations
- Baylor College of Medicine