Papers in the Biological Sciences


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Antimicrobial Agents and Chemotherapy, June 2004, p. 1993–1999 Vol. 48, No. 6


Copyright © 2004, American Society for Microbiology. All Rights Reserved.


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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