Disease relevance of recA

• Interaction of mutagenic spermidine-nitrous acid reaction products with uvr- and recA-dependent repair systems in Salmonella [1].
• However when the same MudI phage is injected by a phage P22 virion, lysogeny is reduced in a recA or recB mutant host [2].
• In a strict anaerobic environment, lack of expression of bacterial recBC function and recA regulatory functions for the SOS repair system is demonstrated by the use of the carcinogenesis-mutagenesis assay and Salmonella phage P22 mutants requiring these host functions for replication [3].
• These compounds were highly toxic but non-mutagenic in the recA- strain, and showed some increased toxicity in polA1- and polA3- strains [4].
• Infection of non-UV-irradiated cells of Salmonella typhimurium with UV-damaged P22 or KB1 phage induces recA-dependent inhibition of cell division, cell mutagenesis and prophage induction but not inhibition of respiration [5].

Psychiatry related information on recA

• To determine the relative importance of these two potentially protective defense mechanisms against oxidative stress encountered by Salmonella during infection of the host, a Salmonella typhimurium double mutant unable to produce either the HPI or HPII catalase was constructed, and compared with an isogenic recA mutant deficient in DNA repair [6].

High impact information on recA

• The recA mutant was hypersusceptible to H2O2 at low cell densities in vitro, while the catalase mutant was more susceptible to high H2O2 concentrations at high cell densities [6].
• The presence of a uvrB mutation or a recA mutation suppressed the generation of spontaneous deletion revertants to approximately 1/2 [7].
• The error-prone repair system encoded in the pKM101 plasmid markedly increased the frequency of total spontaneous reversion events in all genetic backgrounds except recA but did not affect the frequency of spontaneous deletion revertants in any background except polA [7].
• (c) Both recA and recB mutations eliminate inversion formation [8].
• The suppression of the Cym phenotype was recA dependent and frequencies of segregation were affected by UV irradiation [9].

Chemical compound and disease context of recA

• The effects of mutations in the polA and recA genes on mutagenesis by nitrosoguanidine in Salmonella typhimurium [10].
• Results of semi-quantitative plate tests indicated that polA and recA mutants of Salmonella typhimurium strain LT2 trpB1 might be significantly less mutable by nitrosoguanidine (MNNG) than were their repair-proficient parents strains [10].
• Group A compounds (nitracrine and its Cl, F, Me and OMe derivatives) were very toxic to bacteria, and uvrB and recA deletions enhanced toxicity by 10-80-fold [11].
• Thymine starvation of RecA+ Thy- strains of Salmonella typhimurium does not induce the inhibition of cellular respiration, one of the recA-gene dependent SOS functions [12].

Biological context of recA

• Dependence of mutagenesis on the recA gene implicates the action of an error-prone repair system in the fixation of a premutagenic lesion as a mutation [1].
• This mutation caused a slight reduction of ultraviolet resistance but did not affect generalized genetic recombination, indicating that the mutation is different from recA [13].
• A stable O4+ O9+ derivative of a virulent S. enteritidis (O-group D) strain was made by transducing into it first the join point of an appropriate tandem duplication strain, together with the adjacent B.rfb+ gene cluster, and then srl::Tn10 recA [14].
• recA-dependent recombination between rRNA operons generates type II F' plasmids [15].
• Reversion of the hisD3052 (frameshift) mutation, on the other hand, was decreased in both uvrB deletion and recA-type strains [16].

Associations of recA with chemical compounds

• Quantitative data obtained in treat-and-plate experiments showed that this was not the case, at least for low doses of MNNG, and also that the recA strain was significantly more mutable at low doses than its Rec+ parent [10].
• In cultures at a specific stage, proflavine showed decreased mutagenesis in a recA as compared with a wildtupe or uvrB derivative [17].

Other interactions of recA

• One of the two B.rfb+ gene clusters of a (P22-lysogenic) S. typhimurium strain with a tandem duplication of a chromosomal segment including hisD and B.rfb+ was replaced (by transduction) by a D.rfb+ gene cluster; the resulting strain was O1+ O4+ O5+ O9+ and stable as such after being made recA [14].
• Plasmids remain unstable in recA recD recJ mutants; since these do not produce HMW linear concatemers, we propose that a decrease in monomer production leads to plasmid instability. recB recJ strains also display decreased viability, a component of which may be related to their deficiency in DNA repair [18].
• In addition the hyd and recA loci were located establishing the gene order in this region of the chromosome as: pheA tct nalB recA srlA hyd cys [19].

Analytical, diagnostic and therapeutic context of recA

• On the contrary, respiration and ATP concentration are increased after treatment with UV-damaged phage in both RecA+ and RecA- strains, showing that this increase is not recA-dependent [5].

References