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Journal of Bacteriology, September 2000, p. 5202-5210, Vol. 182, No. 18
Department of Microbiology, Cornell
University, Ithaca, New York 14853-8101
Received 17 May 2000/Accepted 30 June 2000
The
0021-9193/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Mutations in Multidrug Efflux Homologs, Sugar
Isomerases, and Antimicrobial Biosynthesis Genes Differentially Elevate
Activity of the
X and
W Factors in
Bacillus subtilis
and
X and
W extracytoplasmic function
sigma factors regulate more than 40 genes in Bacillus
subtilis.
W activates genes which function in
detoxification and the production of antimicrobial compounds, while
X activates functions that modify the cell envelope.
Transposon mutagenesis was used to identify loci which negatively
regulate
W or
X as judged by
up-regulation from the autoregulatory promoter site PW or
PX. Fourteen insertions that activate PW were
identified. The largest class of insertions are likely to affect
transport. These include insertions in genes encoding two multidrug
efflux protein homologs (yqgE and yulE), a
component of the oligopeptide uptake system (oppA), and two
transmembrane proteins with weak similarity to transporters
(yhdP and yueF). Expression from PW is also elevated as a result of inactivation of at least one member of
the
W regulon (ysdB), an ArsR homolog
(yvbA), a predicted rhamnose isomerase (yulE),
and a gene (pksR) implicated in synthesis of difficidin, a
polyketide antibiotic. In a parallel screen, we identified seven
insertions that up-regulate PX. Remarkably, these insertions were in functionally similar genes, including a multidrug efflux homolog (yitG), a mannose-6-phosphate isomerase gene
(yjdE), and loci involved in antibiotic synthesis
(srfAB and possibly yogA and yngK).
Significantly, most insertions that activate PW have little
or no effect on PX, and conversely, insertions that activate PX have no effect on PW. This suggests
that these two regulons respond to distinct sets of molecular signals
which may include toxic molecules which are exported, cell density
signals, and antimicrobial compounds.
*
Corresponding author. Mailing address: Department of
Microbiology, Cornell University, Ithaca, NY 14853-8101. Phone: (607) 255-6570. Fax: (607) 255-3904. E-mail: jdh9{at}cornell.edu.
Present address: School of Life Sciences, Queensland University of
Technology, Brisbane 4001, Australia.
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