| Summary: | <p>Abstract</p> <p>Background</p> <p><it>Enterobacter </it>sp. YSU is resistant to several different heavy metal salts, including selenite. A previous study using M-9 minimal medium showed that when the selenite concentration was 100,000 times higher than the sulfate concentration, selenite entered <it>Escherichia coli </it>cells using two pathways: a specific and a non-specific pathway. In the specific pathway, selenite entered the cells through a yet to be characterized channel dedicated for selenite. In the non-specific pathway, selenite entered the cells through a sulfate permease channel. Addition of L-cystine, an L-cysteine dimer, appeared to indirectly decrease selenite import into the cell through the non-specific pathway. However, it did not affect the level of selenite transport into the cell through the specific pathway.</p> <p>Results</p> <p>Growth curves using M-9 minimal medium containing 40 mM selenite and 1 mM sulfate showed that <it>Enterobacter </it>sp. YSU grew when L-cysteine was present but died when it was absent. Differential protein expression analysis by two dimensional gel electrophoresis showed that CysK was present in cultures containing selenite and lacking L-cysteine but absent in cultures containing both selenite and L-cysteine. Additional RT-PCR studies demonstrated that transcripts for the sulfate permease genes, <it>cysA</it>, <it>cysT </it>and <it>cysW</it>, were down-regulated in the presence of L-cysteine.</p> <p>Conclusion</p> <p>L-cysteine appeared to confer selenite resistance upon <it>Enterobacter sp. </it>YSU by decreasing the level of selenite transport into the cell through the non-specific pathway.</p>
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