Scientists have been aware for many years of genetic programs that get activated 
under stress and produce genetic variants in cells that escape non-proliferating 
conditions. These programs are well conserved in all organisms and expand our 
view of evolution. They mediate genome instability, create diversity in antibody 
formation, expand metabolism and increase fitness of pathogens within host 
environments. Error-prone DNA replication and repair are genetic 
variability-causing agents that get stimulated by the onset of cellular 
stresses. Embedded in these programs is the ability to limit mutagenesis to 
defined genomic regions and times, ensuring integrity of most of the genome. 
Recent evidence suggests that factors involved in RNA polymerase (RNAP) 
processivity or transcriptional derepression contribute to the generation of 
stress-induced mutations. In Bacillus subtilis, transcription-associated 
mutagenesis has been shown to be independent of recombination-dependent repair 
and, in some cases, of the Y DNA polymerases. Central to stationary-phase 
mutagenesis in B. subtilis is the requirement for Mfd, transcription coupling 
repair factor, which suggests a novel mechanism from those described in other 
model systems.