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Browse and analyze data from Al Mamun et al. (Science 2012) Identity and Function of a Large Gene Network Underlying Mutagenic Repair of DNA Breaks 338:1344-1348
This dataset of 93 genes was constructed by screening E. coli for mutants deficient in mutagenic repair of DNA breaks under stress, followed by secondary screens for genes that participate in activation of stress responses. This study identifies a network of genes involved in stress-induced mutagenesis (the SIM Network). This data browser allows you to examine the classification of SIM network genes and explore the data from different assays on individual network genes. You can also download excel versions of the supplemental tables from the paper.
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- All SIM network genes
- SIM network genes upstream of rpoE
- SIM network genes upstream of rpoS
- UV-sensitive SIM network genes upstream of the SOS response
- Essential SIM network genes and promoter mutations
dinB
| Classification | DNA replication and repair |
|---|---|
| Gene-product description | DNA polymerase IV |
| References | PMID:11515498[1] |
| SIM defect strength | Moderate |
| Previously known | Not found [2] |
Mutagenesis Assays | |
| Papillation assay defect (fold-decrease in number of papillae compared with WT) |
4 ± 0.2 |
| Quantitative Lac assay defect (mean fold decrease in mutation rate compared with WT) |
3.3 ± 0.5 [3] |
| Chromosomal Tet assay defect (mean fold decrease in TetR mutant frequency compared with WT) |
5.5 ± 0.75 [4] |
| Chromosomal Nal assay defect (mean fold decrease in NalR mutant frequency compared with WT) |
4.4 ± 1.3 |
Screens for genes upstream of stress responses | |
| σS upstream (% decreases σS activity relative to WT) |
Not |
| Suppressed by mutation in arcB | |
| Suppressed by mutation in arcA | |
| Suppressed by mutation in rssB | |
| Epistatic with rpoS mutation | |
| SDS-EDTA sensitive (σE upstream candidate) |
Not |
| rpoHP3 promoter use defective (σE upstream confirmed; % decreases σE activity relative to WT) |
|
| UV sensitive (SOS response deficient candidate) |
Resistant |
| Spontaneous SOS-deficient | |
| Find more information about dinB via PortEco | |
References
- ↑ Ohmori, H et al. (2001) The Y-family of DNA polymerases. Mol. Cell 8 7-8 PubMed
- ↑ McKenzie, GJ et al. (2001) SOS mutator DNA polymerase IV functions in adaptive mutation and not adaptive amplification. Mol. Cell 7 571-9 PubMed
- ↑ Frisch, RL et al. (2010) Separate DNA Pol II- and Pol IV-dependent pathways of stress-induced mutation during double-strand-break repair in Escherichia coli are controlled by RpoS. J. Bacteriol. 192 4694-700 PubMed
- ↑ Shee, C et al. (2011) Impact of a stress-inducible switch to mutagenic repair of DNA breaks on mutation in Escherichia coli. Proc. Natl. Acad. Sci. U.S.A. 108 13659-64 PubMed
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Back to topExcel versions of supplemental tables:
- Table S03. Stress-induced mutation rates of previously unpublished SIM network mutants in quantitative assay.xlsx
- Table S08. sigmaS activity of catalase-defective mutants.xlsx
- Table S02. Genes of the stress-induced-mutagenesis network.xlsx
- Table S09. Upregulating sigmaS via arcB, arcA or rssB mutations partially restores SIM-proficiency to electron transfer mutants.xlsx
- Table S04. Escherichia coli strains and plasmid used.xlsx
- Table S10. RpoS acts in the same pathway (is epistatic with) electron transfer mutations in DSB-dependent SIM.xlsx
- Table S01. Summary of stress-induced-mutagenesis network genetic analyses.xlsx
- Table S05. Validation of SIM network mutants by Tet and Nal mutation assays.xlsx
- Table S11. sigmaE activity of SDS-EDTA-sensitive mutants.xlsx
- Table S06. Correlations of the magnitudes of SIM-deficiency in four stress-induced mutation assays.xlsx