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J Bacteriol, March 1998, p. 1030-1036, Vol. 180, No. 5
Department of Molecular and Cell Biology,
Institute of Medical Sciences, University of Aberdeen, Foresterhill,
Aberdeen, AB25 2ZD, United Kingdom
Received 3 September 1997/Accepted 20 December 1997
The mechanisms by which Escherichia coli cells survive
exposure to the toxic electrophile N-ethylmaleimide (NEM)
have been investigated. Stationary-phase E. coli cells were
more resistant to NEM than exponential-phase cells. The KefB and KefC
systems were found to play an important role in protecting both
exponential- and stationary-phase cells against NEM. Additionally, RpoS
and the DNA-binding protein Dps aided the survival of both exponential- and stationary-phase cells against NEM. Double mutants lacking both
RpoS and Dps and triple mutants deficient in KefB and KefC and either
RpoS or Dps had an increased sensitivity to NEM in both exponential-
and stationary-phase cells compared to mutants missing only one of
these protective mechanisms. Stationary- and exponential-phase cells of
a quadruple mutant lacking all four protective systems displayed even
greater sensitivity to NEM. These results indicated that protection by
the KefB and KefC systems, RpoS and Dps can each occur independently of
the other systems. Alterations in the level of RpoS in exponentially
growing cells correlated with the degree of NEM sensitivity. Decreasing
the level of RpoS by enriching the growth medium enhanced sensitivity to NEM, whereas a mutant lacking the ClpP protease accumulated RpoS and
gained high levels of resistance to NEM. A slower-growing E. coli strain was also found to accumulate RpoS and had enhanced resistance to NEM. These data emphasize the multiplicity of pathways involved in protecting E. coli cells against NEM.
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Importance of RpoS and Dps in Survival of Exposure
of Both Exponential- and Stationary-Phase Escherichia coli
Cells to the Electrophile N-Ethylmaleimide
*
Corresponding author. Mailing address: Department of
Molecular and Cell Biology, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD, United Kingdom. Phone:
44 1224 273151. Fax: 44 1224 273144. E-mail:
g.p.ferguson{at}abdn.ac.uk.
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