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Thermus thermophilus cells formed siliceous deposits in the presence of supersaturated silicic acid (600 p.p.m SiO(2)). The supersaturated silicic acid promoted interaction between cells and the inside walls of glass culture bottles, leading to the development of cell aggregates or biofilms. Electron probe microanalysis showed that within the aggregates most of the cell surfaces were covered with silica. Under these conditions, there was remarkable production of silica-induced protein (Sip), a solute-binding component of the Fe(3+)-binding ABC transporter. Furthermore, supersaturated silica enhanced resistance to the peptide antibiotics bacitracin, colistin and polymyxin B, which all act on the cell envelope. By contrast, supersaturated silica did not induce resistance to ampicillin, chloramphenicol, kanamycin and tetracycline, which inhibit peptide synthesis. Although strong expression of Sip was detected in liquid cultures of T. thermophilus in the presence of supersaturated silica and colistin, upregulated transcription of putative efflux pump and multidrug resistance ABC transporter genes were not detected by quantitative real-time PCR analysis. These findings suggest Sip promotes silica deposition on the surfaces of cells, after which the silicified outer membrane may serve as a 'suit-of-armor,' conferring resistance to peptide antibiotics.

Silica deposition and phenotypic changes to Thermus thermophilus cultivated in the presence of supersaturated silicia