Coexpression of UmuD' with UmuC suppresses the UV mutagenesis deficiency of groE mutants

2005

J Bacteriol

An insertion in the promoter of the operon that encodes the molecular chaperone GroE was isolated as an antimutator for stationary-phase or adaptive mutation. The groE operon consists of two genes, groES and groEL; point mutations in either gene conferred the same phenotype, reducing Lac ؉ adaptive mutation 10-to 20-fold. groE mutant strains had 1/10 the amount of error-prone DNA polymerase IV (Pol IV). In recG ؉ strains, the reduction in Pol IV was sufficient to account for their low rate of adaptive mutation, but in recG mutant strains, a deficiency of GroE had some additional effect on adaptive mutation. Pol IV is induced as part of the SOS response, but the effect of GroE on Pol IV was independent of LexA. We were unable to show that GroE interacts directly with Pol IV, suggesting that GroE may act indirectly. Together with previous results, these findings indicate that Pol IV is a component of several cellular stress responses.

Section: Discussionmentioning

confidence: 50%

Error-Prone DNA Polymerase IV Is Regulated by the Heat Shock Chaperone GroE in Escherichia coli

Layton

2005

J Bacteriol

“…High levels of epsilon and RNase Hi may also affect DNA repair and mutagenesis by depleting cellular reserves of HSPs. For example, GroEL and GroES stabilize the UmuC protein, which is required for SOS mutagenesis (11). Since GroEL has been shown to act catalytically with DnaK, DnaJ, and GrpE in an in vitro folding pathway (28) (42) and prolonged DNA damage (41).…”

Section: Resultsmentioning

confidence: 99%

Levels of epsilon, an essential replication subunit of Escherichia coli DNA polymerase III, are controlled by heat shock proteins

Marinus

1992

J Bacteriol

In Escherichia coli, epsilon, the proofreading subunit of DNA polymerase III, is encoded by dnaQ. A random search for mutants that affect the expression of dnaQ revealed that mutations in the genes encoding the heat shock proteins (HSPs) DnaK, DnaJ, and GrpE result in dramatic decreases in the cellular levels of epsilon. dnaQ is arranged in an overlapping divergent transcriptional unit with rnhA, which encodes RNase Hi, and mutations in the same HSPs also reduced the apparent levels of RNase Hi. The HSPs had only small effects on transcriptional fusions to these genes; thus, it is likely that they operate primarily at the protein level. Since survival and mutagenesis after DNA damage are affected by epsilon and RNase Hi, HSPs may have a broad influence on various aspects of DNA replication and repair.

“…GroE is required at all temperatures to aid essential proteins to fold and maintain their proper conformation. Levels of DNA Pol V are dependent on GroE because the chaperon interacts with the polymerase subunit of Pol V and protects it from degradation [25]. Recently we found that GroE is also required for normal and induced levels of Pol IV.…”

Section: The Heat-shock Responsementioning

confidence: 99%

Stress responses and genetic variation in bacteria

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

2005

178

106

Under stressful conditions mechanisms that increase genetic variation can bestow a selective advantage. Bacteria have several stress responses that provide ways in which mutation rates can be increased. These include the SOS response, the general stress response, the heat-shock response, and the stringent response, all of which impact the regulation of error-prone polymerases. Adaptive mutation appears to be process by which cells can respond to selective pressure specifically by producing mutations. In Escherichia coli strain FC40 adaptive mutation involves the following inducible components: (i) a recombination pathway that generates mutations; (ii) a DNA polymerase that synthesizes error-containing DNA; and (iii) stress responses that regulate cellular processes. In addition, a subpopulation of cells enters into a state of hypermutation, giving rise to about 10% of the single mutants and virtually all of the mutants with multiple mutations. These bacterial responses have implications for the development of cancer and other genetic disorders in higher organisms.