[Investigation of Bacillus subtilis exolectin ability to modulate the antibiotics effect on growth of Bacillus subtilis mutants].

The ability of Bacillus subtilis exolectin to modulate the effect of antibiotics acting as metabolic inhibitors, which can suppress the biosynthesis of cell wall glycans (ampycillin), replication (mitomycin C) and transcription (rifampycin), have been investigated on mutants of B. subtilis. Extracellular lectin was produced by B. subtilis strains B-7014 isolated from new-born calve's intestines. It was shown that the exolectin displays affinity for to sialic and uronic acids in the decreasing order: mucin, glycuronic acid, N-acetylneuraminic acid, galacturonic acid. It was established by the diffusion method and by determination of minimum inhibitory concentrations (MIC) that B. subtilis exolectin had selective activity as to bacteriostatic effect of antibiotics under study. The activity depended on the antibiotic structure and on mutant genotype defective as to the state of its replication and repair system. The lectin under study had no modulating effect on ampycillin action. There was a tendency to lower the bacteriostatic effect of rifampycin on the growth of strain BD170 (rec+) with the help of exolectin. Only in the case of mitomycin C the significant modulating effect of the bacterial lectin was manifested and its dependence on the mutant genotype was shown. The mutants sensitivity to exolectin effect decreased in the order: BD293 (polC), SB25 (recP), BD224 (recE), BD170 (rec+). Revealed ability of B. subtilis exolectin to protect the action of mitomycin C on growth of mutant BD293 (polC) with defect in the enzyme-DNA polymerase III permits supposing that the process of DNA replication is the most sensitive target for the lectin. The found dependence of modulation of the mitomycin C effect by the bacterial lectin on the genotype of mutants (rec-) demonstrated that the lectin acted following a complex mechanism mediated by a replicative and reparative complex.