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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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barA

Classification Regulators
Gene-product description Sensor kinase of BarA-UvrY two component regulatory system
References PMID:7957084[1]
SIM defect strength Weak
Previously known New

Mutagenesis Assays

Papillation assay defect
(fold-decrease in number of papillae compared with WT)
3 ± 0.4
Quantitative Lac assay defect
(mean fold decrease in mutation rate compared with WT)
2.6 ± 0.7
Chromosomal Tet assay defect
(mean fold decrease in TetR mutant frequency compared with WT)
5 ± 1
Chromosomal Nal assay defect
(mean fold decrease in NalR mutant frequency compared with WT)
6.2 ± 2.3

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
E upstream candidate)
Not
rpoHP3 promoter use defective
E upstream confirmed; % decreases σE activity relative to WT)
UV sensitive
(SOS response deficient candidate)
Resistant
Spontaneous SOS-deficient
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References

  1. Ishige, K et al. (1994) A novel device of bacterial signal transducers. EMBO J. 13 5195-202 PubMed

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Excel versions of supplemental tables: