Genetic Signal Transduction by Nitrosyl-Iron Complexes in Escherichia coli

S. V. Vasilieva^1*, E. Yu. Moshkovskaya¹, N. A. Sanina², S. M. Aldoshin², and A. F. Vanin³

¹Emanuel Institute of Biochemical Physics, Russian Academy of Sciences, ul. Kosygina 4, Moscow 117977, Russia; fax: (7-095) 137-4101; E-mail: svasilieva@polymer.chph.ras.ru

²Institute of Problems of Chemical Physics, Russian Academy of Sciences, Chernogolovka 142432, Moscow Region, Russia; fax: (7-095) 785-7048; E-mail: sanina@icp.ac.ru

³Semenov Institute of Chemical Physics, Russian Academy of Sciences, ul. Kosygina 4, Moscow 117977; fax: (7-095) 938-2156; E-mail: mikoyan@center.chph.ras.ru

^* To whom correspondence should be addressed.

Received July 8, 2003; Revision received November 13, 2003

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Nitrosyl-iron complexes used as aqueous preparations of binuclear dinitrosyl-iron complex with glutathione (DNIC_glu), initially polycrystalline preparations of binuclear tetranitrosyl-iron complex with thiosulfate (TNIC_thio), and also binuclear tetranitrosyl-iron complex with aminotriazole (TNIC_atria) and mononuclear dinitrosyl-iron complex with triazole (DNIC_tria) in the concentration to 0.1 mM activated expression of the soxS and sfiA genes in Escherichia coli. Higher concentrations of polycrystalline preparations of low stability in aqueous solutions were cytotoxic, whereas DNIC_glu, which is more stable in water (up to two days), increased the gene expression on increase in its concentration to 0.5 mM. The iron chelating agent o-phenanthroline completely inhibited the gene expression induced by all compounds studied. The genetic signal transduction seemed to be realized not by nitric oxide molecules and/or iron ions released in solutions but directly by the complexes themselves, which activate transcriptional proteins by transfer onto them of nitrosyl-iron groups [Fe⁺(NO⁺)₂].

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KEY WORDS: nitric oxide, SOS regulon, SoxRS regulon, nitrosyl-iron complexes, Escherichia coli

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