Location
University of Nevada, Las Vegas
Start Date
16-4-2011 10:00 AM
End Date
16-4-2011 11:30 AM
Description
Stationary phase mutagenesis is defined as cellular mechanisms that produce genetic diversity in cells experiencing conditions of stress. These processes are associated with many biological phenomena, including those that produce the formation of cancers in animal cells and other degenerative diseases. Also, these mechanisms are associated with the accumulation of beneficial mutations in bacteria, but follow stochastic processes and are controlled by genetic factors. The current models explaining the generation of stress-induced mutations are predicated on the formation of DNA replication intermediates that are formed during the repair of damaged DNA or during DNA replication and transcription encounters. Here we test the hypothesis that genome (DNA) replication is not required for the generation of stress-induced mutations. Our experiments compared the accumulation of mutations in cells differing in their ability to initiate and elongate genome replication at high temperatures (45° C) and showed that both types of cells accumulate mutations at very similar rates. These results then suggest that resting cells possess replication-independent mechanisms that generate mutations and therefore add novel aspects to our view of the evolutionary process.
Keywords
Mutagenesis; Stress (Physiology)
Disciplines
Cell Biology | Ecology and Evolutionary Biology | Evolution | Genetics and Genomics
Language
English
Embargo Date
6-2-2011
Stationary phase mutagenesis in Bacillus subtilisis independent of genome replication
University of Nevada, Las Vegas
Stationary phase mutagenesis is defined as cellular mechanisms that produce genetic diversity in cells experiencing conditions of stress. These processes are associated with many biological phenomena, including those that produce the formation of cancers in animal cells and other degenerative diseases. Also, these mechanisms are associated with the accumulation of beneficial mutations in bacteria, but follow stochastic processes and are controlled by genetic factors. The current models explaining the generation of stress-induced mutations are predicated on the formation of DNA replication intermediates that are formed during the repair of damaged DNA or during DNA replication and transcription encounters. Here we test the hypothesis that genome (DNA) replication is not required for the generation of stress-induced mutations. Our experiments compared the accumulation of mutations in cells differing in their ability to initiate and elongate genome replication at high temperatures (45° C) and showed that both types of cells accumulate mutations at very similar rates. These results then suggest that resting cells possess replication-independent mechanisms that generate mutations and therefore add novel aspects to our view of the evolutionary process.
Comments
Research supported by NSF grant MCB08443606, and NIH-Nevada INBRE grant 2P20RR016463