PP_3117 encodes ImuA, an accessory component of the LexA2-regulated ImuA-ImuB-DnaE2 damage-tolerance cassette in Pseudomonas putida KT2440. In the closely matched PaW85 background, loss of imuA compromises alkylation-damage tolerance when AlkA repair is absent. Its precise molecular mechanism in this organism remains unresolved. Myxococcus ImuA can bind DNA and hydrolyze ATP, but those measurements have not established the same activities for Q88I84. The specific ImuA assignment distinguishes this protein from the canonical SulA cell-division inhibitor.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0006281 DNA repair | IEA GO_REF:0000118 | MODIFY | Summary: Replace the generic repair interpretation with the supported accessory role in lesion bypass. Reason: The TreeGrafter row stops at generic DNA repair. The ImuA-specific signature and native PaW85/KT2440-matched genetics support its accessory role in DnaE2-mediated lesion tolerance. Translesion synthesis is the mechanistic replacement; current GO does not place it under GO:0006281, so this is a lateral correction of process interpretation rather than an asserted descendant relationship. Generic TLS preserves context-dependent outcomes: ImuC can suppress stationary-phase base substitutions yet promote MMS mutagenesis. Proposed replacements: translesion synthesis 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:17331811 it acted as an anti-mutator in accumulation of base substitution PMID:28118378 ImuB and ImuA are both required for the involvement of ImuC in the DNA alkyl damage tolerance in pseudomonads. |
| GO:0009432 SOS response | IEA GO_REF:0000002 | KEEP AS NON CORE | Summary: ImuA performs accessory work in a LexA2-induced damage-tolerance system. Reason: Retain a bounded SOS-associated effector role, not a sensing or regulatory activity. Direct LexA2 control establishes induction, while native PaW85 ΞimuA genetics and ImuA-specific comparative mechanism independently support functional work in the induced damage-tolerance machinery. Induction alone would not establish participation. The broader TLS role is core; the particular SOS context remains non-core. Supporting Evidence: PMID:15458417 these genes constitute a DNA damage-inducible operon PMID:28118378 ImuB and ImuA are both required for the involvement of ImuC in the DNA alkyl damage tolerance in pseudomonads. |
| GO:0051782 negative regulation of cell division | IEA GO_REF:0000002 | REMOVE | Summary: The specific ImuA assignment contradicts the legacy transfer of canonical SulA division-inhibitor function. Reason: The electronic SulA mapping conflates related but functionally distinct proteins. Q88I84 has the ImuA-specific IPR047610/NCBIfam signature and occupies the LexA2-imuABC cassette; native matched genetics support damage-tolerance accessory function. Canonical SulA inhibits FtsZ assembly, whereas current ImuA evidence concerns the mutasome and, in Myxococcus, DNA binding/ATPase and RecA interaction. Retain removal of the legacy SulA functional assignment on this specific identity basis, without claiming that every conceivable effect on division has been excluded or that no ImuA can affect division indirectly. Supporting Evidence: file:PSEPK/PP_3117/PP_3117-uniprot.txt DR InterPro; IPR047610; ImuA_translesion. file:PSEPK/PP_3117/PP_3117-uniprot.txt DR InterPro; IPR050356; SulA_CellDiv_inhibitor. file:PSEPK/PP_3117/PP_3117-uniprot.txt DR PANTHER; PTHR35369:SF3; TRANSLESION DNA SYNTHESIS-ASSOCIATED PROTEIN IMUA; 1. PMID:9501185 These results indicate that SulA blocks Z ring formation by blocking FtsZ polymerization. |
| GO:0019985 translesion synthesis | ISS file:PSEPK/PP_3117/PP_3117-uniprot.txt | NEW | Summary: ImuA is a cassette-specific accessory protein for DnaE2-dependent lesion bypass. Reason: Retain the historical ISS proposal and payload. ImuA-specific classification plus Caulobacter ortholog genetics support the accessory role. Additional primary evidence now resolves a previously missed native experiment: PMID28118378 deletes PP3117 in PaW85, stated isogenic to KT2440, and finds an alkyl-damage-tolerance defect in ΞalkA. This strengthens physiological support but is not a purified Q88I84 lesion-bypass assay; the historical evidence code is not rewritten. Supporting Evidence: file:PSEPK/PP_3117/PP_3117-uniprot.txt DR InterPro; IPR047610; ImuA_translesion. PMID:15886391 all three genes that compose this expression unit are involved PMID:28118378 ImuB and ImuA are both required for the involvement of ImuC in the DNA alkyl damage tolerance in pseudomonads. |
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Experiment: Purify Q88I84 and test DNA binding and ATP turnover with and without DNA, alongside activity-site controls and pairwise binding to ImuB/RecA. Relate separation-of-function mutants to the established PaW85 alkyl-damage phenotype; do not treat the already published imuA deletion as a missing experiment.
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