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Mercury Inactivates Transcription and the Generalized Transcription Factor TFB in the Archaeon Sulfolobus solfataricus. Vidula Dixit, 2004.Mercury has a long history as an antimicrobial agent effective against eukaryotic and prokaryotic organisms . Despite its prolonged use, the basis for mercury toxicity in prokaryotes is not well understood . Archaea, like bacteria, are prokaryotes but they use a simplified version of the eukaryotic transcription apparatus . This study examined the mechanism of mercury toxicity to the archaeal prokaryote Sulfolobus solfataricus . In vivo challenge with mercuric chloride instantaneously blocked cell division, eliciting a cytostatic response at submicromolar concentrations and a cytocidal response at micromolar concentrations . The cytostatic response was accompanied by a 70% reduction in bulk RNA synthesis and elevated rates of degradation of several transcripts, including tfb-1, tfb-2, and lacS . Whole-cell extracts prepared from mercuric chloride-treated cells or from cell extracts treated in vitro failed to support in vitro transcription of 16S rRNAp and lacSp promoters . Extract-mixing experiments with treated and untreated extracts excluded the occurrence of negative-acting factors in the mercury-treated cell extracts . Addition of transcription factor B (TFB), a general transcription factor homolog of eukaryotic TFIIB, to mercury-treated cell extracts restored >50% of in vitro transcription activity . Consistent with this finding, mercuric ion treatment of TFB in vitro inactivated its ability to restore the in vitro transcription activity of TFB-immunodepleted cell extracts . These findings indicate that the toxicity of mercuric ion in S . solfataricus is in part the consequence of transcription inhibition due to TFB-1 inactivation .
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