About the book
Mutagenesis generates genetic variability for adaptation to changing environments. However, mutagenesis also drives genetic instability phenotypes that confer mitochondrial dysfunction, aging, and carcinogenesis. Organisms have therefore evolved mechanisms to balance accurate replication with mutagenesis. These mechanisms function at the level of DNA replication, post-replication repair, and replication fork stability. DNA polymerases must ensure timely replication while maintaining replication fidelity. Replication fork progression is challenged by DNA damage, which spontaneously occurs but is also inflicted by a multitude of mutagens. Error-prone polymerases and template switch mechanisms allow replication forks to bypass DNA damage. While replication errors can be partially corrected by mismatch repair, mismatch repair proteins, in turn, can drive triplet repeat amplification.
The purpose of this book will be to explore our current understanding of mutagenesis mechanisms. Topics discussed include current knowledge of error-prone polymerases, mismatch repair mechanisms, mutagens, and mutation signatures, spontaneous and induced mutagenesis, transposons, and drug resistance.