ImuA (CC_3213) is an accessory protein encoded by the SOS-regulated imuA-imuB-dnaE2 operon of Caulobacter vibrioides, historically called C. crescentus. In the CB15-derived NA1000 strain, imuA deletion strongly sensitizes cells to mitomycin C and reduces damage-induced mutagenesis, placing it in the DnaE2-dependent damage-tolerance pathway. ImuA has a RecA-like P-loop fold, but its molecular activity and direct interaction partners have not been established in Caulobacter. ATPase and DNA-binding activities measured for Myxococcus ImuA are mechanistic leads rather than demonstrated properties of this protein.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0009432 SOS response | EXP PMID:18083815 Characterization of the SOS regulon of Caulobacter crescentu... | ACCEPT | Summary: ImuA is an effector of the SOS-induced mutagenic damage-tolerance pathway. Reason: The promoter is experimentally LexA regulated, and independent Caulobacter deletion/complementation establishes ImuA participation in damage-induced mutagenesis. GO:0009432 describes an error-prone microbial DNA-damage response, so this is part of the core biological role rather than merely peripheral regulation. Promoter induction alone would not establish protein participation; PMID:15886391 supplies the functional genetic evidence. No LexA protease, transcription-regulatory or RecA-like ATPase activity is implied. Supporting Evidence: PMID:18083815 37 genes regulated in a LexA-dependent manner PMID:18083815 which was confirmed by site-directed mutagenesis studies of the imuA promoter PMID:15886391 The genes imuA and imuB encode previously uncharacterized proteins, which are shown here for the first time to be involved in DNA damage tolerance. |
| GO:0042276 error-prone translesion synthesis | IMP PMID:15886391 An SOS-regulated operon involved in damage-inducible mutagen... | NEW | Summary: An in-frame imuA deletion impairs induced mutagenesis and damage tolerance in the CB15-derived NA1000 strain; the sensitivity phenotype is complemented. Reason: The inherited proposal is retained as the genetically supported cassette process. An in-frame deletion, complementation and controls against downstream polar effects establish a functional requirement for the ImuA protein in the mutagenic tolerance pathway. Similar single-mutant phenotypes and imuB/dnaE2 epistasis support a common pathway, but do not identify ImuA as the nucleotide-inserting enzyme or directly assay bypass of a defined lesion. ImuA is treated as an accessory participant; the exact molecular step remains unresolved. Experiments used NA1000, a CB15 derivative, rather than a separately assayed CB15 culture. Supporting Evidence: PMID:15886391 The genes imuA and imuB encode previously uncharacterized proteins, which are shown here for the first time to be involved in DNA damage tolerance. PMID:15886391 The single mutants imuA, imuB and dnaE2 mutants are extremely sensitive to this condition, revealing that this operon plays a major role in the tolerance to the mit C-induced DNA lesions. PMID:15886391 Both the UV and the mit C sensitivity phenotypes of imuA could be complemented by vector pMR3213, containing the wild-type imuA allele. PMID:15886391 These results confirm that the phenotypes of imuA and imuB strains are not due to negative effects on the expression of downstream genes in the operon. |
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Download this section (compressed HTML)Q: Does Caulobacter ImuA share the DNA-stimulated ATPase and direct ImuB-binding activities measured for Myxococcus ImuA, and which activity is required for native mutagenic damage tolerance?
Experiment: Purify ImuA and test ImuB binding, ssDNA binding and nucleotide hydrolysis, then test separation-of-function alleles for mitomycin C survival and induced mutagenesis in the imuA deletion background.
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