Effects of genetic disruption in thioredoxin and glutathione systems on selenium nanoparticle formation, selenite sensitivity, and selenoprotein biosynthesis in Escherichia coli

Abstract

Escherichia coli uses selenite as a nutritional selenium source for the synthesis of selenoproteins, and excess selenite is converted to elemental selenium nanoparticles (SeNPs) through a detoxification process. The reduction of selenite is thought to be facilitated by two major redox systems: the thioredoxin (Trx) system and glutathione (GSH) system. However, the extent to which these redox systems are involved in selenoprotein synthesis and SeNP formation remains unclear. In this study, we investigated the effects of gene disruption in the Trx (trxA, trxB, and trxC) and GSH (gshB and gor) systems on SeNP formation, selenite sensitivity, and selenoprotein synthesis in E. coli. We found that the disruption of a single gene in either the Trx or GSH system did not drastically affect SeNP formation via selenite reduction in the presence of 1 mM selenite. However, trxB, gshB, and gor were observed to be important for the tolerance of the bacterium to > 5 mM selenite. The ΔtrxA and ΔtrxB strains exhibited lower activity of the selenoprotein formate dehydrogenase as compared to the wild-type strain, suggesting that trxA and trxB are important for selenoprotein biosynthesis. Selenite detoxification via SeNP formation involves both the Trx and GSH systems, but selenoprotein biosynthesis specifically depends on the Trx system.

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